Unstriated and unstriped muscle, one of the muscles of the internal organs, blood vessels, hair follicles, etc. Contractile elements are elongated, usually spindle-shaped cells with centrally located nuclei. Smooth muscle fibers are bound together into sheets or bundles by reticular fibers and frequently elastic nets are also abundant. (From Stedman, 25th ed)
A process leading to shortening and/or development of tension in muscle tissue. Muscle contraction occurs by a sliding filament mechanism whereby actin filaments slide inward among the myosin filaments.
The nonstriated involuntary muscle tissue of blood vessels.
Non-striated, elongated, spindle-shaped cells found lining the digestive tract, uterus, and blood vessels. They are derived from specialized myoblasts (MYOBLASTS, SMOOTH MUSCLE).
A group of intracellular-signaling serine threonine kinases that bind to RHO GTP-BINDING PROTEINS. They were originally found to mediate the effects of rhoA GTP-BINDING PROTEIN on the formation of STRESS FIBERS and FOCAL ADHESIONS. Rho-associated kinases have specificity for a variety of substrates including MYOSIN-LIGHT-CHAIN PHOSPHATASE and LIM KINASES.
A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.
A diverse superfamily of proteins that function as translocating proteins. They share the common characteristics of being able to bind ACTINS and hydrolyze MgATP. Myosins generally consist of heavy chains which are involved in locomotion, and light chains which are involved in regulation. Within the structure of myosin heavy chain are three domains: the head, the neck and the tail. The head region of the heavy chain contains the actin binding domain and MgATPase domain which provides energy for locomotion. The neck region is involved in binding the light-chains. The tail region provides the anchoring point that maintains the position of the heavy chain. The superfamily of myosins is organized into structural classes based upon the type and arrangement of the subunits they contain.
The physiological narrowing of BLOOD VESSELS by contraction of the VASCULAR SMOOTH MUSCLE.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
The main trunk of the systemic arteries.
Organic chemistry methodology that mimics the modular nature of various biosynthetic processes. It uses highly reliable and selective reactions designed to "click" i.e., rapidly join small modular units together in high yield, without offensive byproducts. In combination with COMBINATORIAL CHEMISTRY TECHNIQUES, it is used for the synthesis of new compounds and combinatorial libraries.
Elements of limited time intervals, contributing to particular results or situations.
Deposition of calcium into the blood vessel structures. Excessive calcification of the vessels are associated with ATHEROSCLEROTIC PLAQUES formation particularly after MYOCARDIAL INFARCTION (see MONCKEBERG MEDIAL CALCIFIC SCLEROSIS) and chronic kidney diseases which in turn increase VASCULAR STIFFNESS.
A naturally occurring phenomenon where terminally differentiated cells dedifferentiate to the point where they can switch CELL LINEAGES. The cells then differentiate into other cell types.
Pathologic deposition of calcium salts in tissues.
The formation of cartilage. This process is directed by CHONDROCYTES which continually divide and lay down matrix during development. It is sometimes a precursor to OSTEOGENESIS.
Proteins that are coded by immediate-early genes, in the absence of de novo protein synthesis. The term was originally used exclusively for viral regulatory proteins that were synthesized just after viral integration into the host cell. It is also used to describe cellular proteins which are synthesized immediately after the resting cell is stimulated by extracellular signals.
A member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23.
The tendency of a phenomenon to recur at regular intervals; in biological systems, the recurrence of certain activities (including hormonal, cellular, neural) may be annual, seasonal, monthly, daily, or more frequently (ultradian).
An element in the alkali group of metals with an atomic symbol K, atomic number 19, and atomic weight 39.10. It is the chief cation in the intracellular fluid of muscle and other cells. Potassium ion is a strong electrolyte that plays a significant role in the regulation of fluid volume and maintenance of the WATER-ELECTROLYTE BALANCE.
General increase in bulk of a part or organ due to CELL ENLARGEMENT and accumulation of FLUIDS AND SECRETIONS, not due to tumor formation, nor to an increase in the number of cells (HYPERPLASIA).
An octapeptide that is a potent but labile vasoconstrictor. It is produced from angiotensin I after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME. The amino acid in position 5 varies in different species. To block VASOCONSTRICTION and HYPERTENSION effect of angiotensin II, patients are often treated with ACE INHIBITORS or with ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKERS.
An enzyme that catalyzes the active transport system of sodium and potassium ions across the cell wall. Sodium and potassium ions are closely coupled with membrane ATPase which undergoes phosphorylation and dephosphorylation, thereby providing energy for transport of these ions against concentration gradients.
A group of enzymes that catalyzes the hydrolysis of terminal, non-reducing beta-D-galactose residues in beta-galactosides. Deficiency of beta-Galactosidase A1 may cause GANGLIOSIDOSIS, GM1.
Genetically developed small pigs for use in biomedical research. There are several strains - Yucatan miniature, Sinclair miniature, and Minnesota miniature.
Constituent composed of protein and phospholipid that is widely distributed in many tissues. It serves as a cofactor with factor VIIa to activate factor X in the extrinsic pathway of blood coagulation.
A strong oxidizing agent used in aqueous solution as a ripening agent, bleach, and topical anti-infective. It is relatively unstable and solutions deteriorate over time unless stabilized by the addition of acetanilide or similar organic materials.
A class of lipoproteins of small size (18-25 nm) and light (1.019-1.063 g/ml) particles with a core composed mainly of CHOLESTEROL ESTERS and smaller amounts of TRIGLYCERIDES. The surface monolayer consists mostly of PHOSPHOLIPIDS, a single copy of APOLIPOPROTEIN B-100, and free cholesterol molecules. The main LDL function is to transport cholesterol and cholesterol esters to extrahepatic tissues.
Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)
Application of principles and practices of engineering science to biomedical research and health care.
A technique of culturing mixed cell types in vitro to allow their synergistic or antagonistic interactions, such as on CELL DIFFERENTIATION or APOPTOSIS. Coculture can be of different types of cells, tissues, or organs from normal or disease states.
An element with atomic symbol Cd, atomic number 48, and atomic weight 114. It is a metal and ingestion will lead to CADMIUM POISONING.
A cadmium halide in the form of colorless crystals, soluble in water, methanol, and ethanol. It is used in photography, in dyeing, and calico printing, and as a solution to precipitate sulfides. (McGraw-Hill Dictionary of Scientific and Technical Terms, 5th ed)
Poisoning occurring after exposure to cadmium compounds or fumes. It may cause gastrointestinal syndromes, anemia, or pneumonitis.
The smallest divisions of the arteries located between the muscular arteries and the capillaries.
A strain of Rattus norvegicus with elevated blood pressure used as a model for studying hypertension and stroke.

Chlamydial and human heat shock protein 60s activate human vascular endothelium, smooth muscle cells, and macrophages. (1/15014)

Both chlamydial and human heat shock protein 60s (HSP 60), which colocalize in human atheroma, may contribute to inflammation during atherogenesis. We tested the hypothesis that chlamydial or human HSP 60 activates human endothelial cells (ECs), smooth muscle cells (SMCs), and monocyte-derived macrophages. We examined the expression of adhesion molecules such as endothelial-leukocyte adhesion molecule-1 (E-selectin), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1), and the production of the proinflammatory cytokine interleukin-6 (IL-6). We also tested whether either HSP 60 induces nuclear factor-kappaB (NF-kappaB), which contributes to the gene expression of these molecules. Either chlamydial or human HSP 60 induced E-selectin, ICAM-1, and VCAM-1 expression on ECs similar to levels induced by Escherichia coli lipopolysaccharide (LPS). Each HSP 60 also significantly induced IL-6 production by ECs, SMCs, and macrophages to an extent similar to that induced by E. coli LPS, as assessed by enzyme-linked immunosorbent assay (ELISA). In ECs, either HSP 60 triggered activation of NF-kappaB complexes containing p65 and p50 Rel proteins. Heat treatment abolished all these effects, but did not alter the ability of E. coli LPS to induce these functions. Chlamydial and human HSP 60s therefore activate human vascular cell functions relevant to atherogenesis and lesional complications. These findings help to elucidate the mechanisms by which a chronic asymptomatic chlamydial infection might contribute to the pathophysiology of atheroma.  (+info)

Endothelial cells modulate the proliferation of mural cell precursors via platelet-derived growth factor-BB and heterotypic cell contact. (2/15014)

Embryological data suggest that endothelial cells (ECs) direct the recruitment and differentiation of mural cell precursors. We have developed in vitro coculture systems to model some of these events and have shown that ECs direct the migration of undifferentiated mesenchymal cells (10T1/2 cells) and induce their differentiation toward a smooth muscle cell/pericyte lineage. The present study was undertaken to investigate cell proliferation in these cocultures. ECs and 10T1/2 cells were cocultured in an underagarose assay in the absence of contact. There was a 2-fold increase in bromodeoxyuridine labeling of 10T1/2 cells in response to ECs, which was completely inhibited by the inclusion of neutralizing antiserum against platelet-derived growth factor (PDGF)-B. Antisera against PDGF-A, basic fibroblast growth factor, or transforming growth factor (TGF)-beta had no effect on EC-stimulated 10T1/2 cell proliferation. EC proliferation was not influenced by coculture with 10T1/2 cells in the absence of contact. The cells were then cocultured so that contact was permitted. Double labeling and fluorescence-activated cell sorter analysis revealed that ECs and 10T1/2 cells were growth-inhibited by 43% and 47%, respectively. Conditioned media from contacting EC-10T1/2 cell cocultures inhibited the growth of both cell types by 61% and 48%, respectively. Although we have previously shown a role for TGF-beta in coculture-induced mural cell differentiation, growth inhibition resulting from contacting cocultures or conditioned media was not suppressed by the presence of neutralizing antiserum against TGF-beta. Furthermore, the decreased proliferation of 10T1/2 cells in the direct cocultures could not be attributed to downregulation of the PDGF-B in ECs or the PDGF receptor-beta in the 10T1/2 cells. Our data suggest that modulation of proliferation occurs during EC recruitment of mesenchymal cells and that heterotypic cell-cell contact and soluble factors play a role in growth control during vessel assembly.  (+info)

Anti-monocyte chemoattractant protein-1/monocyte chemotactic and activating factor antibody inhibits neointimal hyperplasia in injured rat carotid arteries. (3/15014)

Monocyte chemoattractant protein-1 (MCP-1)/monocyte chemotactic and activating factor (MCAF) has been suggested to promote atherogenesis. The effects of in vivo neutralization of MCP-1 in a rat model were examined in an effort to clarify the role of MCP-1 in the development of neointimal hyperplasia. Competitive polymerase chain reaction analysis revealed maximum MCP-1 mRNA expression at 4 hours after carotid arterial injury. Increased immunoreactivities of MCP-1 were also detected at 2 and 8 hours after injury. Either anti-MCP-1 antibody or nonimmunized goat IgG (10 mg/kg) was then administered every 12 hours to rats that had undergone carotid arterial injury. Treatment with 3 consecutive doses of anti-MCP-1 antibody within 24 hours (experiment 1) and every 12 hours for 5 days (experiment 2) significantly inhibited neointimal hyperplasia at day 14, resulting in a 27.8% reduction of the mean intima/media ratio (P<0.05) in experiment 1 and a 43.6% reduction (P<0.01) in experiment 2. This effect was still apparent at day 56 (55.6% inhibition; P<0.05). The number of vascular smooth muscle cells in the neointima at day 4 was significantly reduced by anti-MCP-1 treatment, demonstrating the important role of MCP-1 in early neointimal lesion formation. However, recombinant MCP-1 did not stimulate chemotaxis of vascular smooth muscle cells in an in vitro migration assay. These results suggest that MCP-1 promotes neointimal hyperplasia in early neointimal lesion formation and that neutralization of MCP-1 before, and immediately after, arterial injury may be effective in preventing restenosis after angioplasty. Further studies are needed to clarify the mechanism underlying the promotion of neointimal hyperplasia by MCP-1.  (+info)

Vascular remodeling in response to altered blood flow is mediated by fibroblast growth factor-2. (4/15014)

Vascular structures adapt to changes in blood flow by adjusting their diameter accordingly. The factors mediating this process are only beginning to be identified. We have recently established a mouse model of arterial remodeling in which flow in the common carotid artery is interrupted by ligation of the vessel near the carotid bifurcation, resulting in a dramatic reduction in vessel diameter as a consequence of inward remodeling and intimal lesion formation. In the present study, we used this model to determine the role of fibroblast growth factor-2 (FGF-2) in the remodeling response by maintaining neutralizing serum levels of a mouse monoclonal antibody against FGF-2 for 4 weeks. Morphometric analysis revealed that intimal lesion formation was not affected by the antibody. However, lumen narrowing was significantly inhibited, resulting in a greater than 3-fold increase in lumen area in anti-FGF-2-treated animals compared with controls. Treatment with anti-FGF-2 antibody significantly inhibited the reduction in vessel diameter (inward remodeling) and shortening of the internal elastic lamina in the ligated vessel. In addition, anti-FGF-2 treatment also caused outward remodeling of the contralateral carotid artery. These findings identify FGF-2 as an important factor in vascular remodeling, and its effects are likely to be mediated by increasing vascular tone. The results are consistent with the recent observation of reduced vascular tone in the FGF-2-deficient mouse.  (+info)

Induction of serotonin transporter by hypoxia in pulmonary vascular smooth muscle cells. Relationship with the mitogenic action of serotonin. (5/15014)

-The increased delivery of serotonin (5-hydroxytryptamine, 5-HT) to the lung aggravates the development of hypoxia-induced pulmonary hypertension in rats, possibly through stimulation of the proliferation of pulmonary artery smooth muscle cells (PA-SMCs). In cultured rat PA-SMCs, 5-HT (10(-8) to 10(-6) mol/L) induced DNA synthesis and potentiated the mitogenic effect of platelet-derived growth factor-BB (10 ng/mL). This effect was dependent on the 5-HT transporter (5-HTT), since it was prevented by the 5-HTT inhibitors fluoxetine (10(-6) mol/L) and paroxetine (10(-7) mol/L), but it was unaltered by ketanserin (10(-6) mol/L), a 5-HT2A receptor antagonist. In PA-SMCs exposed to hypoxia, the levels of 5-HTT mRNA (measured by competitive reverse transcriptase-polymerase chain reaction) increased by 240% within 2 hours, followed by a 3-fold increase in the uptake of [3H]5-HT at 24 hours. Cotransfection of the cells with a construct of human 5-HTT promoter-luciferase gene reporter and of pCMV-beta-galactosidase gene allowed the demonstration that exposure of cells to hypoxia produced a 5.5-fold increase in luciferase activity, with no change in beta-galactosidase activity. The increased expression of 5-HTT in hypoxic cells was associated with a greater mitogenic response to 5-HT (10(-8) to 10(-6) mol/L) in the absence as well as in the presence of platelet-derived growth factor-BB. 5-HTT expression assessed by quantitative reverse transcriptase-polymerase chain reaction and in situ hybridization in the lungs was found to predominate in the media of pulmonary artery, in which a marked increase was noted in rats that had been exposed to hypoxia for 15 days. These data show that in vitro and in vivo exposure to hypoxia induces, via a transcriptional mechanism, 5-HTT expression in PA-SMCs, and that this effect contributes to the stimulatory action of 5-HT on PA-SMC proliferation. In vivo expression of 5-HTT by PA-SMC may play a key role in serotonin-mediated pulmonary vascular remodeling.  (+info)

Tissue factor pathway inhibitor-2 is a novel mitogen for vascular smooth muscle cells. (6/15014)

A mitogen for growth-arrested cultured bovine aortic smooth muscle cells was purified to homogeneity from the supernatant of cultured human umbilical vein endothelial cells by heparin affinity chromatography and reverse-phase high performance liquid chromatography. This mitogen was revealed to be tissue factor pathway inhibitor-2 (TFPI-2), which is a Kunitz-type serine protease inhibitor. TFPI-2 was expressed in baby hamster kidney cells using a mammalian expression vector. Recombinant TFPI-2 (rTFPI-2) stimulated DNA synthesis and cell proliferation in a dose-dependent manner (1-500 nM). rTFPI-2 activated mitogen-activated protein kinase (MAPK) activity and stimulated early proto-oncogene c-fos mRNA expression in smooth muscle cells. MAPK, c-fos expression and the mitogenic activity were inhibited by a specific inhibitor of MAPK kinase, PD098059. Thus, the mitogenic function of rTFPI-2 is considered to be mediated through MAPK pathway. TFPI has been reported to exhibit antiproliferative action after vascular smooth muscle injury in addition to the ability to inhibit activation of the extrinsic coagulation cascade. However, structurally similar TFPI-2 was found to have a mitogenic activity for the smooth muscle cell.  (+info)

RNA antisense abrogation of MAT1 induces G1 phase arrest and triggers apoptosis in aortic smooth muscle cells. (7/15014)

The human MAT1 gene (menage a trois 1) is an assembly factor and a targeting subunit of cyclin-dependent kinase (CDK)-activating kinase. The novel mechanisms by which MAT1 forms an active CDK-activating kinase and determines substrate specificity of CDK7-cyclin H are involved in the cell cycle, DNA repair, and transcription. Hyperplasia of vascular smooth muscle cells (SMC) is a fundamental pathologic feature of luminal narrowing in vascular occlusive diseases, and nothing is yet known regarding the cell cycle phase specificity of the MAT1 gene in its involvement in SMC proliferation. To investigate such novel regulatory pathways, MAT1 expression was abrogated by retrovirus-mediated gene transfer of antisense MAT1 RNA in cultured rat aortic SMCs. We show that abrogation of MAT1 expression retards SMC proliferation and inhibits cell activation from a nonproliferative state. Furthermore, we have demonstrated that these effects are due to G1 phase arrest and apoptotic cell death. Our studies indicate a link between cell cycle control and apoptosis and reveal a potential mechanism for coupling the regulation of MAT1 with G1 exit and prevention of apoptosis.  (+info)

JunB forms the majority of the AP-1 complex and is a target for redox regulation by receptor tyrosine kinase and G protein-coupled receptor agonists in smooth muscle cells. (8/15014)

To understand the role of redox-sensitive mechanisms in vascular smooth muscle cell (VSMC) growth, we have studied the effect of N-acetylcysteine (NAC), a thiol antioxidant, and diphenyleneiodonium (DPI), a potent NADH/NADPH oxidase inhibitor, on serum-, platelet-derived growth factor BB-, and thrombin-induced ERK2, JNK1, and p38 mitogen-activated protein (MAP) kinase activation; c-Fos, c-Jun, and JunB expression; and DNA synthesis. Both NAC and DPI completely inhibited agonist-induced AP-1 activity and DNA synthesis in VSMC. On the contrary, these compounds had differential effects on agonist-induced ERK2, JNK1, and p38 MAP kinase activation and c-Fos, c-Jun, and JunB expression. NAC inhibited agonist-induced ERK2, JNK1, and p38 MAP kinase activation and c-Fos, c-Jun, and JunB expression except for platelet-derived growth factor BB-induced ERK2 activation. In contrast, DPI only inhibited agonist-induced p38 MAP kinase activation and c-Fos and JunB expression. Antibody supershift assays indicated the presence of c-Fos and JunB in the AP-1 complex formed in response to all three agonists. In addition, cotransfection of VSMC with expression plasmids for c-Fos and members of the Jun family along with the AP-1-dependent reporter gene revealed that AP-1 with c-Fos and JunB composition exhibited a higher transactivating activity than AP-1 with other compositions tested. All three agonists significantly stimulated reactive oxygen species production, and this effect was inhibited by both NAC and DPI. Together, these results strongly suggest a role for redox-sensitive mechanisms in agonist-induced ERK2, JNK1, and p38 MAP kinase activation; c-Fos, c-Jun, and JunB expression; AP-1 activity; and DNA synthesis in VSMC. These results also suggest a role for NADH/NADPH oxidase activity in some subset of early signaling events such as p38 MAP kinase activation and c-Fos and JunB induction, which appear to be important in agonist-induced AP-1 activity and DNA synthesis in VSMC.  (+info)

TY - JOUR. T1 - The mechanisms of uremic serum-induced expression of bone matrix proteins in bovine vascular smooth muscle cells. AU - Chen, N. X.. AU - Duan, D.. AU - ONeill, K. D.. AU - Wolisi, G. O.. AU - Koczman, J. J.. AU - LaClair, R.. AU - Moe, S. M.. PY - 2006/9/1. Y1 - 2006/9/1. N2 - We have previously found that uremic human serum upregulates RUNX2 in vascular smooth muscle cells (VSMCs), and that RUNX2 is upregulated in areas of vascular calcification in vivo. To confirm the role of RUNX2, we transiently transfected a dominant-negative RUNX2 (ΔRUNX2) construct in bovine vascular smooth muscle cells (BVSMCs). Blocking RUNX2 transcriptional activity significantly decreased uremic serum induced alkaline phosphatase (ALP) activity (268 ± 34 vs 188 ± 9.5 U/g protein, P , 0.05) and osteocalcin expression (172 ± 17 vs 125 ± 9 ODU, P , 0.05). To determine the mechanism by which uremic serum upregulates RUNX2, we examined cell signaling pathways. BVSMCs were incubated in the presence or ...
TY - JOUR. T1 - Glucose alters platelet-derived growth factor-BB activity in human aortic vascular smooth muscle cells by stimulating protein phosphatase 2A in a protein kinase C-beta II-dependent pathway. AU - Campbell, Malcolm. AU - Trimble, Elizabeth. PY - 2004/9. Y1 - 2004/9. M3 - Article. VL - 47. SP - A445-A445. JO - Diabetologia. JF - Diabetologia. SN - 0012-186X. ER - ...
TY - JOUR. T1 - Long-term zinc deprivation accelerates rat vascular smooth muscle cell proliferation involving the down-regulation of JNK1/2 expression in MAPK signaling. AU - Alcantara, Ethel H.. AU - Shin, Mee Young. AU - Feldmann, Jörg AU - Nixon, Graeme F.. AU - Beattie, John H.. AU - Kwun, In Sook. PY - 2013/5/1. Y1 - 2013/5/1. N2 - Background: The accelerated proliferation of vascular smooth muscle cells (VSMCs) is a contributor for atherosclerosis by thickening the vascular wall. Since zinc modulation of VSMC proliferation has not been clarified, this study investigated whether zinc affects VSMC proliferation. Methods and results: Both a rat aorta origin vascular smooth muscle cell line (A7r5 VSMCs) and primary VSMCs which were collected from rat aorta (pVSMCs) were cultured with zinc (0-50 µM Zn) for short- (=12 d) and long-term (28 d) periods under normal non-calcifying (0 or 1 mM P) or calcifying (,2 mM P) P conditions. Mouse vascular endothelial cells (MS I cells) were also cultured ...
Hello. I need to culture bovine aortic smooth muscle cell. I do not know what medium should be used. What supplements or growth factors are required? In how much in amount? Please give me some help. Thanks in advance ...
Mouse Aortic Vascular Smooth Muscle Cells from Creative Bioarray are isolated from tissue of New Zealand White Rabbits. Rabbits Aortic Vascular Smooth Muscle Cells are grown in T25 tissue culture flasks pre-coated with gelatin-based solution for 0.5 hour and incubated in Creative Bioarrays Cell Culture Medium generally for 3-7 days. Cultures are then expanded. Prior to shipping, cells are detached from flasks and immediately cryo-preserved in vials. Each vial contains at least 1x10^6 cells per ml and is delivered frozen ...
The purpose of the present investigation was to explore the effects of well-defined flow conditions on the activity of tissue factor (TF) expressed on the surface of cultured rat vascular smooth muscle cells. Cells were cultured to confluence on Permanox brand slides and stimulated to express TF by a 90 min incubation with fresh growth medium containing 10 percent calf serum. The stimulated cells were then placed in a parallel plate flow chamber and perfused with Hanks Balanced Salt Solution containing factor VIIa, factor X (FX), and calcium. The chamber effluent was collected and assayed for factor Xa (FXa) and the steady-state flux of FXa was calculated. The flux values were 68.73, 94.81, 139.75, 138.19, 316.82, and 592.92 fmole/min/cm2 at wall shear rates of 10, 20, 40, 80, 320, and 1280 s−1 respectively. The FXa flux depended on the wall shear rate to a greater degree than predicted by classical mass transport theory. The flux at each shear rate was three to five times less than that ...
TY - JOUR. T1 - Down-regulation of superoxide dismutase gene expression in cultured rat aortic smooth muscle cells (A7r5) after long-term incubation with vitamin C. AU - Liu, J. C.. AU - Chow, J. M.. AU - Tsai, M. F.. AU - Hsieh, M. H.. AU - Chen, Y. J.. AU - Chan, P.. PY - 2000. Y1 - 2000. N2 - Background: Oxygen free radicals have been linked to the process of cardiovascular disease and aging. Epidemiological studies supported the beneficial effect of supplementation of antioxidants such as vitamin C and vitamin E. Superoxide dismutase (SOD) is a endogenous enzyme system which can scavenge oxygen free radicals. This study investigated the effect of supplementation of ascorbic acid (vitamin C) on the changes of SOD. Methods: Rat aortic smooth muscle cells (A7r5) were divided into 4 groups: a control group (without vitamin C) and treatment groups with vitamin C at 50 μM, 100 μM and 200 μM. After a short-term (2 days) or long-term (7 days) incubation, the enzyme activity and mRNA level of SOD ...
Isoliquiritigenin (ISL) has various biological activities including as antioxidant and an inhibitor of PI3K/AKT signaling pathway. However, both oxidative stress and activated PI3K/AKT signaling contribute to the aberrant proliferation of vascular smooth muscle cells (VSMCs). This study is aimed to explore the effect of ISL on the proliferation of human arterial smooth muscle cells (HASMCs) and to investigate the underlying mechanisms. BrdU incorporation, cell cycle and reactive oxygen species (ROS) in normal or ISL treated HASMCs were analyzed by flow cytometry. Cell viablity was measured by CCK-8. Protein expression levels were examined by Western blot, and superoxide dismutase (SOD) activity was detected by using commercial kit. We observed that ISL could inhibit the proliferation of HASMCs in a dose and time dependent manner. Cell cycle of ISL treated HASMCs arrested mainly in G1/S phase and accompanied with elevated expression of p27 and decreased expression of CyclinD1 and CyclinE. In addition,
Isoliquiritigenin (ISL) has various biological activities including as antioxidant and an inhibitor of PI3K/AKT signaling pathway. However, both oxidative stress and activated PI3K/AKT signaling contribute to the aberrant proliferation of vascular smooth muscle cells (VSMCs). This study is aimed to explore the effect of ISL on the proliferation of human arterial smooth muscle cells (HASMCs) and to investigate the underlying mechanisms. BrdU incorporation, cell cycle and reactive oxygen species (ROS) in normal or ISL treated HASMCs were analyzed by flow cytometry. Cell viablity was measured by CCK-8. Protein expression levels were examined by Western blot, and superoxide dismutase (SOD) activity was detected by using commercial kit. We observed that ISL could inhibit the proliferation of HASMCs in a dose and time dependent manner. Cell cycle of ISL treated HASMCs arrested mainly in G1/S phase and accompanied with elevated expression of p27 and decreased expression of CyclinD1 and CyclinE. In addition,
These findings point to a role of LTB4 in atherosclerosis and intimal hyperplasia, by identifying the vascular SMC as targets for this potent chemotactic molecule. The expression of the human BLT1 receptor on vascular SMC was demonstrated by immunohistochemical stainings of arterial samples, as well as in cultured human coronary SMC by Western blotting and RT-PCR. Together, these findings provide evidence that human vascular SMC express BLT1 receptors in vivo as well as in vitro, and they suggest that these cells may represent an additional target for LTB4.. Patch-clamp analysis and functional studies of SMC clarified that BLT1 receptors transduce a signal that leads to important functional responses in human vascular SMC. Membrane currents in human coronary artery SMC were increased significantly in the presence of either LTB4 or the selective BLT1 receptor partial agonist U75302. Also, another characteristic pharmacological feature of the BLT1 receptor (namely, its rapid desensitization by an ...
TY - JOUR. T1 - Nitric oxide reversibly inhibits the migration of cultured vascular smooth muscle cells. AU - Sarkar, Rajabrata. AU - Meinberg, Eric G.. AU - Stanley, James C.. AU - Gordon, R. David. AU - Webb, R Clinton. PY - 1996/1/1. Y1 - 1996/1/1. N2 - Augmentation of nitric oxide (NO) production in vivo decreases lesions in a variety of models of arterial injury, and inhibition of NO synthase exacerbates experimental intimal lesions. Both vascular smooth muscle cell (VSMC) proliferation and migration contribute to lesion formation. Although NO inhibit VSMC proliferation, its effects on VSMC migration are unknown. To test the hypothesis that NO inhibits VSMC migration independent of inhibition of proliferation, we examined migration of rat aortic VSMCs after wounding of a confluent culture in the presence of chemical donors of NO. Hydroxyurea was used to eliminate any confounding effect of NO on proliferation. Three NO donors, diethylamine NONOate, spermine NONOate, and S-nitrosoglutathione, ...
The concept of arterial SMC heterogeneity has gained wide acceptance in the last years.1 2 33 The distinct phenotypes of arterial SMCs have been mainly identified in vitro,4 5 6 7 8 9 10 11 12 13 14 15 16 suggesting that specific features of SMC populations arise and are maintained in the particular environment of cell culture. Hence, it was of interest to investigate whether in vitro SMC phenotypes are preserved when SMCs are placed back in an in vivo environment. For this purpose, we have implanted 2 SMC populations exhibiting distinct levels of differentiation in vitro into the rat carotid artery submitted to endothelial injury.24 25 The implanted SMCs were marked with PKH-26, a lipophilic cell membrane linker that is halved with each cell division but is not lost from the cell membrane.34 Our results show that the 2 implanted populations essentially retain for 20 days in vivo the phenotype that they specifically exhibited in vitro.. Spindle-shaped and epithelioid rat SMC populations have ...
TY - JOUR. T1 - A 310-bp minimal promoter mediates smooth muscle cell-specific expression of telokin. AU - Smith, Aiping F.. AU - Bigsby, Robert M.. AU - Word, R. Ann. AU - Herring, B. Paul. PY - 1998/5/1. Y1 - 1998/5/1. N2 - A cell-specific promoter located in an intron of the smooth muscle myosin light chain kinase gene directs transcription of telokin exclusively in smooth muscle cells. Transgenic mice were generated in which a 310-bp rabbit telokin promoter fragment, extending from -163 to +147, was used to drive expression of simian virus 40 large T antigen. Smooth muscle-specific expression of the T-antigen transgene paralleled that of the endogenous telokin gene in all smooth muscle tissues except uterus. The 310-bp promoter fragment resulted in very low levels of transgene expression in uterus; in contrast, a transgene driven by a 2.4-kb fragment (-2250 to +147) resulted in high levels of transgene expression in uterine smooth muscle. Telokin expression levels correlate with the estrogen ...
Methods and Results-Ex vivo optical imaging confirmed that Id3−/− Ldlr−/− mice have significantly fewer aortic B cells than Id3+/+ Ldlr−/− mice. After 8 and 16 weeks of Western diet, Id3−/− Ldlr−/− mice developed significantly more atherosclerosis than Id3+/+ Ldlr−/− mice, with Id3+/− Ldlr−/− mice demonstrating an intermediate phenotype. There were no differences in serum lipid levels between genotypes. Immunostaining demonstrated that aortas from Id3−/− Ldlr−/− mice had greater intimal macrophage density and C-C chemokine ligand 20 and vascular cell adhesion molecule 1 (VCAM-1) expression compared with Id3+/+ Ldlr−/− mice. Real-time polymerase chain reaction demonstrated increased VCAM-1 mRNA levels in the aortas of Id3−/− Ldlr−/− mice. Primary vascular smooth muscle cells from Id3−/− mice expressed greater amounts of VCAM-1 protein compared with control. Gain and loss of function studies in primary vascular smooth muscle cells identified a ...
With cardiovascular disease (CVD) being the leading cause of morbidity and death in the United States and worldwide (2, 28), studying the mechanisms of these pathologies is imperative. Recent studies have shown that a correlation exists between the activation of synthetic and growth-promoting transforming growth factor-β1 (TGF-β1) and the pathogenesis of CVD (13). Cell-to-cell adhesion through components of the extracellular matrix (ECM) is required for normal growth conditions; however, these adhesive interactions have also been linked to CVD pathogenesis. TGF-β1 is thought to synthesize ECM elements through a Smad3-dependent pathway. Considering the correlation between TGF-β1 and CVD, studying its mechanistic effects on cell proliferation and migration could prove beneficial in combatting CVD pathologies. Past studies involving TGF-β1 have generally focused on its intracellular Smad3 signals, and results have shown conflicting effects of Smad3 and even it switching between pro-growth and ...
Citation: Kumari, R. et al. (2003) ATP and UTP responses of cultured rat aortic smooth muscle cells revisited: Dominance of P2Y2 receptors. British Journal of Pharmacology, 140 (7), pp. 1169-1176. ...
Vascular smooth muscle cells contribute to the formation of atherosclerotic plaques by proliferating in response to vascular injury and releasing growth-promoting factors. Because their autocrine and paracrine effects are not fully understood, expression of such growth factor genes in specific cell types in vivo would help to determine their mechanism of action. We describe a method to transfer vascular smooth muscle cells expressing recombinant gene products to localized segments of the arterial wall. Vascular smooth muscle cells from the inbred Yucatan minipig were infected in vitro with an amphotropic, replication-defective retrovirus transducing the gene for Escherichia coli beta-galactosidase. Vascular smooth muscle cells expressing this recombinant gene were implanted, using a catheter, into denuded iliofemoral artery segments of pigs in vivo. These arteries subsequently demonstrated beta-galactosidase activity in cells of the intima and media. This method, which provides for the ...
Atherosclerosis is an inflammatory disease that is characterised by the involvement of chemokines that are important for the recruitment of leukocytes and scavenger receptors that mediate foam cell formation. Several cytokines are involved in the regulation of chemokines and scavenger receptors in atherosclerosis. CXCL16 is a chemokine and scavenger receptor and found in macrophages in human atherosclerotic lesions. Using double-labelled immunohistochemistry, we identified that smooth muscle cells in human lesions express CXCL16. We then analysed the effects of IFN-gamma, TNF-alpha, IL-12, IL-15, IL-18, and LPS on CXCL16 expression in cultured aortic smooth muscle cells. IFN-gamma was the most potent CXCL16 inducer and increased mRNA, soluble form, membrane form, and total cellular levels of CXCL16. The IFN-gamma induction of CXCL16 was also associated with increased uptake of oxLDL into these cells. Taken together, smooth muscle cells express CXCL16 in atherosclerotic lesions, which may play a ...
TY - JOUR. T1 - Potential roles of tyrosine phosphatase mkp-1 in the proliferation of rat vascular smooth muscle cells. AU - Lai, K.. AU - Wang, H.. AU - Lee, W. S.. AU - Lee, M. E.. AU - Haber, E.. PY - 1996. Y1 - 1996. N2 - The proliferation and migration of arterial smooth muscle cells plays an important role in the pathological process of arteriosclerosis. A number of cytokines and growth factors are upregulated and bind to their respective receptors, which in turn activate multiple signal transduction pathways leading ultimately to the activation of MAP kinases. These kinases in turn relay signals to the nucleus that result in activation of the previously quiescent smooth muscle cell. The activity of MAP kinases is countered by phosphatases. In this report we investigate the potential role of a dual tyrosine phosphatase, MAP kinase phosphatase 1 (MKP-1), in the proliferation of smooth muscle cells. We show that MKP-1 is highly expressed in vascular tissues. In situ hybridization ...
The present study examined age-related changes in the vascular relaxation response to adenine nucleotides in hypertensive and normotensive rats. Aortic ring segments from normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR), age 4-6, 9-10, and 13-14 weeks, were examined for relaxation to adenosine 5-triphosphate (ATP). The extent of ATP-induced relaxation in aortic ring segments with intact endothelium was unchanged with advancing age. Rubbed (endothelium-denuded) ring preparations at the age of 4-6 weeks showed a dose-dependent relaxation similar to that of the unrubbed rings. With advancing age, the ATP-induced relaxation in the rubbed rings decreased and was abolished. The relaxation response did not differ between the SHR and WKY animals at any age, whether the preparations were rubbed or unrubbed. The stable ATP analogue beta,r-methylene ATP induced a relaxation response similar to ATP in rubbed rings at 4-6 weeks of age. In addition, treatment with ...
TY - JOUR. T1 - Modulation of collagen synthesis by tumor necrosis factor alpha in cultured vascular smooth muscle cells. AU - Hiraga, Syouichi. AU - Kaji, Toshiyuki. AU - Ueda, Yoshimichi. AU - Zisaki, Fumiko. AU - Iwata, Kazushi. AU - Koizumi, Fumitomo. AU - Okada, Yasunori. AU - Katsuda, Shogo. AU - Nakanishi, Isao. PY - 1999/12/10. Y1 - 1999/12/10. N2 - Collagen synthesis in vascular smooth muscle cells (SMCs) after exposure to tumor necrosis factor alpha (TNF-α) was investigated using a culture system. The synthesis of collagenase-digestible proteins (CDP) and noncollagenous proteins (NCP) was evaluated by the [3H]proline incorporation. It was shown that TNF-α markedly suppresses the incorporation of [3H]proline into both CDP and NCP in confluent cultures of SMCs but not in sparse cultures of the cells. Such a marked suppression by TNF-α was not observed in confluent bovine aortic endothelial cells and human fibroblastic IMR-90 cells. In confluent SMCs, the synthesis of CDP was more ...
TY - JOUR. T1 - Biphasic effect of p21Cip1 on smooth muscle cell proliferation: Role of PI 3-kinase and Skp2-mediated degradation. AU - Bond, M. AU - Sala-Newby, GB. AU - Wu, Y-J. AU - Newby, AC. N1 - Publisher: Elsevier. PY - 2006/1. Y1 - 2006/1. U2 - 10.1016/j.cardiores.2005.08.020. DO - 10.1016/j.cardiores.2005.08.020. M3 - Article (Academic Journal). VL - 69 (1). SP - 198. EP - 206. JO - Cardiovascular Research. JF - Cardiovascular Research. SN - 0008-6363. ER - ...
Vascular smooth muscle (VSM) cell proliferation contributes to the pathogenesis of atherosclerosis, restenosis after angioplasty and vein graft disease. The regulation of genes involved in VSM cell proliferation, particularly by naturally occurring inhibitors, is therefore of some importance. We have investigated the role of the c-myc proto-oncogene in growth arrest of exponentially proliferating rat VSM cells, following mitogen withdrawal, treatment with heparin (50 micrograms/ml), interferon-gamma (IFN-gamma) (100 i.u./ml), or the cyclic nucleotide analogues, 8-bromo-adenosine-3′5′-cyclic monophosphate (8-Br-cAMP; 0.1 mM) and 8-bromoguanosine-3′5′-cyclic monophosphate (8-Br-cGMP; 0.1 mM). Growth arrest was accompanied by down-regulation of c-Myc protein and mRNA following treatment with all inhibitors. Serum withdrawal or IFN-gamma treatment suppressed c-myc expression by more than 50% within 2 h, and this occurred throughout the cell cycle. Platelet-derived growth factor, epidermal ...
I am planning to set up a co-culture system for human endothelial cells and human VASCULAR smooth muscle cells. I would be really interested to find out about methods of extraction and primary culture of human vascular smooth muscle cells, if anyone can help and advise, please mail me! Thanks Pippa Deex ...
Vascular smooth muscle refers to the particular type of smooth muscle found within, and composing the majority of the wall of blood vessels. Vascular smooth muscle refers to the particular type of smooth muscle found within, and composing the majority of the wall of blood vessels. Vascular smooth muscle is innervated primarily by the sympathetic nervous system through adrenergic receptors (adrenoceptors). The three types of adrenoceptors present are: α 1 {\displaystyle \alpha _{1}} , α 2 {\displaystyle \alpha _{2}} and β 2 {\displaystyle \beta _{2}} . The main endogenous agonist of these cell receptors is norepinephrine (NE). The adrenergic receptors exert opposite physiologic effects in the vascular smooth muscle under activation: α 1 {\displaystyle \alpha _{1}} receptors. Under NE binding α 1 {\displaystyle \alpha _{1}} receptors cause vasoconstriction (i.e. contraction of the vascular smooth muscle cells decreasing the diameter of the vessels). α 1 {\displaystyle \alpha _{1}} receptors ...
292653345 - EP 1085880 A2 2001-03-28 - USE OF ALKYLATING COMPOUNDS FOR INHIBITING PROLIFERATION OF ARTERIAL SMOOTH MUSCLE CELLS - [origin: WO9963981A2] The present invention provides methods and compositions for inhibiting the proliferation of smooth muscle cells at a site of vascular injury. The methods include intravascular administration of a reactive compound to the site of injury, without the requirement for activation or sustained release of the compound.[origin: WO9963981A2] The present invention provides methods and compositions for inhibiting the proliferation of smooth muscle cells at a site of vascular injury. The methods include intravascular administration of a reactive compound to the site of injury, without the requirement for activation or sustained release of the compound.
TY - JOUR. T1 - 170 Mitochondrial-dependent signalling in vascular smooth muscle cell proliferation. AU - Al-Sulti, Zuhair. AU - Kingsmore, David. AU - Coats, Paul. PY - 2014/6. Y1 - 2014/6. N2 - UNLABELLED: A hallmark of vascular disease is the cellular adaptive response characterised by proliferation and migration. Although many studies have identified the signalling pathways involved in cell proliferation and migration (p38, p44/42 MAP Kinase and JNK), the mechanisms initiating cell de-differentiation, proliferation/ apoptosis and migration are yet to be fully elucidated. Mitochondria are one of the organelles that have received growing attention in vascular and pulmonary vascular proliferative disease.(1) Mitochondria are classically known to be responsible for cellular energy production. However growing evidence suggests a role in cell de-differentiation and the fine balance between cell apoptosis and proliferation.(2) The aim of this work was to expand our understanding of the potential ...
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TY - JOUR. T1 - Norepinephrine sensitivity and membrane potentials of caudal arterial muscle in doca-salt, dahl, and shr hypertension in the rat. AU - Hermsmeyer, Kent. AU - Abel, Peter W.. AU - Trapani, Angelo J.. PY - 1982/5. Y1 - 1982/5. N2 - Comparison of norepinephrine (NE) sensitivity in caudal arterial muscle of rats with three forms of hypertension showed that there was no increase in either DOCA-salt or Dahl genetic hypertension, in contrast to the increased NE sensitivity found in spontaneously hypertensive rats (SHR). In hypertension induced by deoxycorticosterone acetate (DOCA)-salt treatment, as in Dahl genetic hypertension, there was also no difference in membrane potential (Em) between hypertensive and normotensive rats. By comparison to the SHR membrane alterations reported previously, any increased NE sensitivity might have been associated with altered Em electrogenesis which is triggered by a trophic factor of the sympathetic nervous system. SHR have a lower intracellular K+ ...
Proliferation and migration of vascular smooth muscle cells (VSMCs) play crucial roles in the development of vascular restenosis. Our previous study showed that CCN4, namely Wnt1 inducible signaling pathway protein 1 (WISP1), significantly promotes proliferation and migration of rat VSMCs, but its mechanism remains unclear. This study aims to investigate whether and how WISP1 stimulates proliferation and migration of human VSMCs. Western blot analysis showed that FBS treatment increased WISP1 protein levels in human VSMCs in a dose-dependent manner. Overexpression of WISP1 using adenovirus encoding WISP1 (AD-WISP1) significantly increased proliferation rate of human VSMCs by 2.98-fold compared with empty virus (EV)-transfected cells, shown by EdU incorporation assay. Additionally, Scratch-induced wound healing assay revealed that adenovirus-mediated overexpression of WISP1 significantly increased cell migration compared with EV-transfected cells from 6h (4.56±1.14% vs. 11.23±2.25%, P,0.05) to ...
Diabetic Mouse Brain Vascular Smooth Muscle Cells from Creative Bioarray are isolated from the brain vessel of Diabetic (db/db) mice (8 weeks). Diabetic Mouse Brain Vascular Smooth Muscle Cells are grown in T25 tissue culture flasks pre-coated with gelatin-based coating solution for 2 min and incubated in Creative Bioarrays Culture Complete Growth Medium generally for 3-7 days. Prior to shipping, cells at passage 1 are detached from the culture flasks and immediately cryo-preserved in vials. Each vial contains at least 0.5x10^6cells per ml and is delivered frozen ...
To investigate potential interactions between angiotensin II (AII) and the insulin signaling system in the vasculature, insulin and AII regulation of insulin receptor substrate-1 (IRS-1) phosphorylation and phosphatidylinositol (PI) 3-kinase activation were examined in rat aortic smooth muscle cells …
Fingerprint Dive into the research topics of Effects of carvedilol alone and in the presence of cyclosporine A on the DNA synthesis of cultured vascular smooth muscle cells. Together they form a unique fingerprint. ...
BioAssay record AID 421037 submitted by ChEMBL: Inhibition of PDGF-BB-stimulated Rac1 activity in human aortic smooth muscle cells assessed as reduction of ratio of Rac1GTP/Rac1 levels at 25 uM after 4 hrs by pull-down assay.
The present study may have important pathological and therapeutic implications because overgrowth of VSMCs is a pivotal etiologic factor in the development of atherosclerosis and restenosis after angioplasty.26-28 To date, inhibiting VSMC proliferation is among the most effective strategies for preventing their overgrowth and controlling neointimal thickening.14 Previous studies have shown that targeting Ras with negative regulators or blocking the Ras downstream pathways is able to effectively attenuate restenosis from balloon catheterization.14,15,29-33 Our recent studies have demonstrated that rMfn-2 is a powerful endogenous Ras inhibitor and that somatic gene transfer of rMfn-2 profoundly inhibits rat VSMC proliferation and balloon injury-induced neointima thickening in vivo by inhibiting the Ras-Raf-MEK-ERK/MAPK signaling pathway.17. In addition to inhibition of cell proliferation, growing evidence has indicated that apoptosis also plays an essential role in the control of neointimal ...
Aortic calcification was demonstrated in experimental animal models of hyperhomocysteinemia. Mild hyperhomocysteinemia was associated with aortic calcification, suggesting a relationship between homocysteine (HCY) and the pathogenesis of aortic calcification. In the present study, the effect of HCY on vascular calcification was examined in calcifying and non-calcifying vascular smooth muscle cells (VSMCs). Cell calcification was induced by incubation of VSMCs with [ glycerophosphate. Proliferation of VSMCs was studied by cell counting, H-3-thymidine (H-3-TdR) and H-3-leucine (H-3-Leu) incorporation. Ca-45 accumulation, cell calcium content, and alkaline phosphatase (ALP) activity were measured as indices of calcification. The results showed that the proliferation of calcifying VSMCs, which was indicated by cell counting, H-3-TdR and H-3-Leu incorporation in calcifying VSMCs, was enhanced as compared with that of non-calcifying VSMCs. HCY promoted increases in cell number, H-3-TdR and H-3-Leu ...
Diabetic complications largely affect the circulation and are associated with resistance to insulin and altered levels of insulin-like growth factor-I (IGF-I). Insulin resistance and altered IGF-I levels are also associated with vascular disease. Insulin and IGF-I are highly homologous peptides and can cross react with each others respective receptors, insulin receptors (IR) and IGF-I receptors (IGFIR), which also share homology to a large extent and can form hybrid IR/IGF-IR. Cultured endothelial and vascular smooth muscle cells from different vascular beds express considerably more IGF-IR than IR. Since the direct action of insulin and IGFs on the vasculature remains poorly understood, our aim was to study mechanisms behind insulin resistance and IGF-I sensitivity and the possible impact of hybrid IR/IGF-IR in vascular cells.. This thesis is based on four papers investigating the presence of IR and IGF-IR in cultured endothelial and vascular smooth muscle cells, and in tissue specimens from ...
TY - GEN. T1 - Curvature-induced spontaneous detachment of vascular smooth muscle cell sheets. T2 - Towards vascular self assembly in microchannels. AU - Yamashita, Tadahiro. AU - Kollmannsberger, P.. AU - Mawatari, K.. AU - Vogel, V.. AU - Kitamori, T.. PY - 2013/1/1. Y1 - 2013/1/1. N2 - A new model is proposed which describes the spontaneous detachment of vascular smooth muscle cells induced by surface curvature. Growing tubular structures from smooth muscle cells (SMCs) in vitro is a key challenge in microvascular tissue engineering. SMC growth is however significantly suppressed on curved substrates. We show that this is caused by mechanical interaction between adhering cells and the surrounding geometry, which compromises the adhesion of growing tissue. Our model opens up new strategies for engineering luminal vasculature in microdevices, and gives new insights for controlling tissue formation in micro environments.. AB - A new model is proposed which describes the spontaneous detachment of ...
BACKGROUND: Pathological vascular remodeling in venous bypass grafts (VGs) results in smooth muscle cell (SMC) intimal hyperplasia and provides the substrate for progressive atherosclerosis, the principal cause of late VG failure. Nitric oxide (NO) bioactivity is reduced in VGs, in association with increased vascular superoxide production, but how these features relate to pathological VG remodeling remains unclear. We used gene transfer of the neuronal isoform of nitric oxide synthase (nNOS) to investigate how increased NO production modulates vascular remodeling in VGs and determined the effects on late VG phenotype. METHODS AND RESULTS: New Zealand White rabbits (n=60) underwent jugular-carotid interposition bypass graft surgery with intraoperative adenoviral gene transfer of nNOS or beta-galactosidase. Vessels were analyzed after 3 days (early, to investigate acute injury/inflammation) or 28 days (late, to investigate SMC intimal hyperplasia). In early VGs, nNOS gene transfer significantly increased
Abstract. Vascular smooth muscle cells (SMC) are a major cell type comprising the walls of blood vessels. We report the synthesis of granulocyte colony- stimula
MicroRNAs (miRNAs) are an emerging class of highly conserved, non-coding small RNAs that regulate gene expression at the post-transcriptional level. Recent findings have shown that miR-1 and miR-133 play a critical role in cardiogenesis and cardiomyocyte hypertrophy. However, the role of miR-1 and miR-133 in vascular disease is currently unknown. Thus, the aim of the present study was to evaluate the role, if any, of miR-1 and miR-133 in vascular smooth muscle cell (VSMC) growth in vitro and in vivo. miR-1 and miR-133 transcripts were evaluated by quantitative real-time polymerase chain reaction (qRT-PCR) in quiescent vs. proliferating VSMCs in vitro and in vivo. VSMC were transfected in culture dishes with adenoviral vector constructs carrying miR-1 or miR133. VSMC proliferation was measured by Brdu incorporation. VSMC apoptosis was induced by H2O2 and measured by a Tdt assay. In the in vivo protocol, balloon injury of the right carotid was produced in male Wistar rats. Straight after the ...
Little, Peter J., Ballinger, Mandy L., Survase, Soniya, Osman, Narin, Ogru, Esra, Geytenbeek, Stephen, Bruemmer, Dennis and Nigro, Julie (2008) Phosphorylated troglitazone activates PPAR gamma and inhibits vascular smooth muscle cell proliferation and proteoglycan synthesis. Journal of Cardiovascular Pharmacology, 51 3: 274-279. ...
Fingerprint Dive into the research topics of Mesenchymal stem cells expressing eNOS and a Cav1 mutant inhibit vascular smooth muscle cell proliferation in a rat model of pulmonary hypertension. Together they form a unique fingerprint. ...
MicroRNAs (miRNAs) have been identified as important participants in the development of atherosclerosis (AS). The present study explored the role of miR-128-3p in the dysfunction of vascular smooth muscle cells (VSMCs) and the underlying mechanism. Human VSMCs and ApoE knockout (ApoE−/−) C57BL/6J mice were used to establish AS cell and animal models, respectively. Expression levels of miR-128-3p, forkhead box O4 (FOXO4) and matrix metallopeptidase 9 (MMP9) were detected using qRT-PCR and Western blot, respectively. CCK-8, BrdU, and Transwell assays as well as flow cytometry analysis were performed to detect the proliferation, migration and apoptosis of VSMCs. Levels of inflammatory cytokines and lipids in human VSMCs, mice serum and mice VSMCs were also determined. The binding site between miR-128-3p and 3′UTR of FOXO4 was confirmed using luciferase reporter gene assay. MiR-128-3p was found to be decreased in AS patient serum, ox-LDL-treated VSMCs, AS mice serum and VSMCs of AS mice. Transfection
Objective: Peroxisome proliferator-activated receptor γ (PPARγ) agonists reduce blood pressure (BP) and vascular injury in hypertensive rodents and humans. Pparγ inactivation in vascular smooth muscle cells (VSMC)using a tamoxifen inducible Cre-Lox system enhanced angiotensin II-induced vascular injury. Transgenic mice overexpressing endothelin (ET)-1selectively in the endothelium (eET-1) exhibit endothelial dysfunction, increased oxidative stress and inflammation. We hypothesized that inactivation of Pparγ in VSMC(smPparγ-/-)will exaggerate ET-1-induced vascular damage.. Methods and Results: Elevenweek-old male control, eET-1, smPparγ-/-and eET-1/smPparγ-/- mice weretreated with tamoxifen (1 mg/kg/day, s.c.) for 5 days and sacrificed 4 weeks later. Systolic BP was higher in eET-1compared to control (123±5 vs 109±2 mmHg,P,0.05)and unaffected by Pparγ inactivation.Mesenteric artery (MA) vasodilatory responses to acetylcholine were impaired only in smPparγ-/- (P,0.05) compared to ...
The recognition that cells of the vascular wall can secrete cytokines such as IL-1 suggests new mechanisms for initiating or sustaining inflammatory responses in blood vessels. We report that purified human monocyte-derived IL-1 or recombinant human IL-1 (rIL-1 beta and rIL-1 alpha) induce cultured human smooth muscle cells derived from veins or arteries to synthesize IL-1 beta mRNA and produce and release biologically active IL-1. rIL-1 beta also stimulated the production of PGE2 by smooth muscle cells. Exposure to rIL-1 beta (1-100 ng/ml), or rIL-1 alpha (0.01-10 ng/ml) increased IL-1 beta mRNA levels within 30 min. Actinomycin D (1 microgram/ml) prevented the induction of IL-1 beta mRNA by rIL-1. IL-1 alpha mRNA was detected in SMC treated with cycloheximide (1 microgram/ml) and rIL-1 beta, or cycloheximide alone. rIL-1 alpha and rIL-1 beta produced maximal levels of IL-1 beta mRNA after 4 h, and intracellular IL-1 biological activity after 6 h of exposure. Release of IL-1 activity in the ...
OBJECTIVE: Cerebral aneurysm is a common vascular disease with high morbidity and mortality. Vascular smooth muscle deletion or dysplasia is an important r
How is Bovine Anterior Cerebral Arterial Smooth Muscle Cells abbreviated? BACASMC stands for Bovine Anterior Cerebral Arterial Smooth Muscle Cells. BACASMC is defined as Bovine Anterior Cerebral Arterial Smooth Muscle Cells very rarely.
TY - JOUR. T1 - N-cadherin-dependent cell-cell contacts promote human saphenous vein smooth muscle cell survival. AU - Koutsouki, Evgenia. AU - Beeching, Cressida A. AU - Slater, Sadie C. AU - Blaschuk, Orest W. AU - Sala-Newby, Graciela B. AU - George, Sarah J. PY - 2005/5. Y1 - 2005/5. N2 - OBJECTIVE: Vascular smooth muscle cell (VSMC) apoptosis is thought to contribute to atherosclerotic plaque instability. Cadherin mediates calcium-dependent homophilic cell-cell contact. We studied the role of N-cadherin in VSMC apoptosis.METHODS AND RESULTS: Human saphenous vein VSMCs were grown in agarose-coated wells to allow cadherin-mediated aggregate formation. Cell death and apoptosis were determined after disruption of cadherins using several approaches (n, or =3 per approach). Calcium removal from culture medium or addition of nonspecific cadherin antagonist peptides significantly decreased aggregate formation and increased cell death by apoptosis (34+/-6% versus 75+/-1% and 19+/-1% versus 40+/-5%, ...
TY - JOUR. T1 - Steroid sensitivity of norepinephrine uptake by human bronchial arterial and rabbit aortic smooth muscle cells. AU - Horvath, G.. AU - Lieb, T.. AU - Conner, G. E.. AU - Salathe, M.. AU - Wanner, A.. PY - 2001. Y1 - 2001. N2 - We have shown that an inhaled glucocorticosteroid (GS) causes α1-adrenergic antagonist-blockable, rapid, and transient bronchial vasoconstriction in healthy and asthmatic subjects. Steroids inhibit norepinephrine (NE) uptake by non-neuronal cells, thereby increasing NE concentration at α-adrenergic receptor sites. This could explain the GS-induced bronchial vasoconstriction. We therefore studied expression of the steroid-sensitive extraneuronal monoamine transporter (EMT) and steroid sensitivity of NE uptake in human bronchial artery and rabbit aorta (as a substitute for the limited supply of human bronchial artery). NE uptake was measured using a semiquantitative, sucrose-potassium phosphate-glyoxylic acid fluorescence method that we newly adapted for ...
BACKGROUND: Apoptosis of vascular cells is considered to be a major determinant of atherosclerotic plaque vulnerability and potential rupture. Plasmin can be generated in atherosclerotic plaques and recent in vitro data suggest that plasminogen activation may trigger vascular smooth muscle cell (VSMC) apoptosis. AIM: To determine whether plasminogen activation may induce aortic VSMC apoptosis ex vivo and in vivo. METHODS AND RESULTS: Mice with single or combined deficiencies of apolipoprotein E (ApoE) and plasminogen activator inhibitor-1 (PAI-1) were used. Ex vivo incubation with plasminogen of isolated aortic tunica media from PAI-1-deficient mice induced plasminogen activation and VSMC apoptosis, which was inhibited by alpha2-antiplasmin. In vivo, levels of plasmin, active caspase 3 and VSMC apoptotic index were significantly higher in atherosclerotic aortas from mice with combined ApoE and PAI-1 deficiencies than in those from littermates with single ApoE deficiency. A parallel decrease in VSMC
TY - JOUR. T1 - Interaction of methylglyoxal and hydrogen sulfide in rat vascular smooth muscle cells. AU - Chang, Tuanjie. AU - Untereiner, Ashley. AU - Liu, Jianghai. AU - Wu, Lingyun. PY - 2010/5/1. Y1 - 2010/5/1. N2 - Hydrogen sulfide (H2S) is a gasotransmitter with multifaceted physiological functions, including the regulation of glucose metabolism. Methylglyoxal (MG) is an intermediate of glucose metabolism and plays an important role in the pathogenesis of insulin resistance syndromes. In the present study, we investigated the effect of MG on H2S synthesis and the interaction between these two endogenous substances. In cultured vascular smooth muscle cells (VSMCs), MG (10, 30, and 50μM) significantly decreased cellular H2S levels in a concentration-dependent manner, while H 2S donor, NaHS (30, 60, and 90μM), significantly decreased cellular MG levels. The expression level and activity of H2S- producing enzyme, cystathionine γ-lyase (CSE), were significantly decreased by MG treatment. ...
TY - JOUR. T1 - Down-regulation of protein kinase c inhibits insulin-like growth factor i-induced vascular smooth muscle cell proliferation, migration, and gene expression. AU - Yano, K.. AU - Bauchat, J. R.. AU - Liimatta, M. B.. AU - Clemmons, D. R.. AU - Duan, C.. N1 - Copyright: Copyright 2018 Elsevier B.V., All rights reserved.. PY - 1999. Y1 - 1999. N2 - Insulin-like growth factor-I (IGF-I) plays an important role in regulating vascular smooth muscle cell (VSMC) proliferation, directed migration, differentiation, and apoptosis. The signaling mechanisms used by IGF-I to elicit these actions, however, are not well defined. In this study, we examined the role(s) of protein kinase C (PKC) in mediating the IGF-I actions in cultured porcine VSMCs. Out of the eleven known members of PKC family, PKC-α, -βI, -ε, -η, -λ, θ, and -ζ were detectable by Western immunoblot analysis in these cells. Further analysis indicated that the subcellular distribution of several PKC isoforms is regulated by ...
Bilirubin is a heme metabolite generated by the concerted action of the enzymes heme oxygenase and biliverdin reductase. Although long considered a toxic byproduct of heme catabolism, recent preclinical, and clinical studies indicate the bilirubin exerts beneficial effects in the circulation. In the present study, we determined whether local administration of bilirubin attenuates neointima formation following injury of rat carotid arteries. In addition, the ability of bilirubin to regulate the proliferation and migration of human arterial smooth muscle cells (SMCs) was investigated. Local perivascular administration of bilirubin immediately following balloon injury of rat carotid arteries significantly attenuated neointima formation. Bilirubin-mediated inhibition of neointimal thickening was associated with a significant decrease in ERK activity and cyclin D1 and A protein expression, and an increase in p21 and p53 protein expression in injured blood vessels. Treatment of human aortic SMCs with ...
Cardiac hypertrophy triggered by mechanical load possesses features in common with growth factor signal transduction. A hemodynamic load provokes rapid expression of the growth factor-inducible nuclear oncogene, c-fos, and certain peptide growth factors specifically stimulate the fetal cardiac genes associated with hypertrophy, even in the absence of load. These include the gene encoding vascular smooth muscle alpha-actin, the earliest alpha-actin expressed during cardiac myogenesis; however, it is not known whether reactivation of the smooth muscle alpha-actin gene occurs in ventricular hypertrophy. We therefore investigated myocardial expression of the smooth muscle alpha-actin gene after hemodynamic overload. Smooth muscle alpha-actin mRNA was discernible 24 h after coarctation and was persistently expressed for up to 30 d. In hypertrophied hearts, the prevalence of smooth muscle alpha-actin gene induction was 0.909, versus 0.545 for skeletal muscle alpha-actin (P less than 0.05). ...
TY - JOUR. T1 - Cellular and molecular effects of hyperglycemia on ion channels in vascular smooth muscle. AU - Nieves-Cintrón, Madeline. AU - Flores-Tamez, Víctor A.. AU - Le, Thanhmai. AU - Baudel, Miguel Martín Aragón. AU - Navedo, Manuel F.. PY - 2020. Y1 - 2020. N2 - Diabetes affects millions of people worldwide. This devastating disease dramatically increases the risk of developing cardiovascular disorders. A hallmark metabolic abnormality in diabetes is hyperglycemia, which contributes to the pathogenesis of cardiovascular complications. These cardiovascular complications are, at least in part, related to hyperglycemia-induced molecular and cellular changes in the cells making up blood vessels. Whereas the mechanisms mediating endothelial dysfunction during hyperglycemia have been extensively examined, much less is known about how hyperglycemia impacts vascular smooth muscle function. Vascular smooth muscle function is exquisitely regulated by many ion channels, including several ...
We investigated the effect of the potassium channel opener pinacidil on ATP-dependent K+ channels (KATP) in the relaxation of porcine and human coronary arteries by means of isometric contraction experiments in arterial rings. We also measured whole cell currents in freshly isolated porcine and human coronary artery vascular smooth muscle cells with patch clamp. We first characterized serotonin-induced precontractions in our vessels and proved that the contractions were mediated by Ca2+ influx through voltage-dependent Ca2+ channels. Similarly, we observed that serotonin-induced contractions were strongly enhanced by small K(+)-induced depolarizations. Pinacidil completely relaxed rings preconstricted with 5 microM serotonin and produced dose-dependent relaxations of 5 microM serotonin-preconstricted rings, with an IC50 of 1.26 microM. Similar results were observed (IC50 = 1.15 microM) when the endothelium was removed. The KATP blocker glibenclamide (3 microM), inhibited pinacidil-induced ...
Vascular smooth muscle cell (VSMC) proliferation in response to hyperglycemia is an important process in the development of arterial vessel hyperplasia. The shape change of mitochondria is dynamic and closely related to fission and fusion. Hydrogen sulfide (H2S) was confirmed to have anti-oxidative, anti-inflammatory and anti-proliferative effects. However, little it is known about its effects on mitochondrial morphology induced by hyperglycemia. The aim of the study is to demonstrate that H2S inhibits VSMC proliferation through regulating mitochondrial fission. We observe lower H2S levels as well as higher proliferative protein expression levels for proliferative cell nuclear antigen (PCNA) and cyclin D1 and higher mitochondrial fusion-fission protein expression levels for dynamin-related protein 1 (Drp 1) in human kidney arteries and in db/db mouse aorta. Exogenous H2S (100 μM NaHS) inhibits vascular smooth muscle cells of human pulmonary aorta(HPASMC) proliferation and migration in response to high
Vascular smooth muscle cell (VSMC) proliferation in response to hyperglycemia is an important process in the development of arterial vessel hyperplasia. The shape change of mitochondria is dynamic and closely related to fission and fusion. Hydrogen sulfide (H2S) was confirmed to have anti-oxidative, anti-inflammatory and anti-proliferative effects. However, little it is known about its effects on mitochondrial morphology induced by hyperglycemia. The aim of the study is to demonstrate that H2S inhibits VSMC proliferation through regulating mitochondrial fission. We observe lower H2S levels as well as higher proliferative protein expression levels for proliferative cell nuclear antigen (PCNA) and cyclin D1 and higher mitochondrial fusion-fission protein expression levels for dynamin-related protein 1 (Drp 1) in human kidney arteries and in db/db mouse aorta. Exogenous H2S (100 μM NaHS) inhibits vascular smooth muscle cells of human pulmonary aorta(HPASMC) proliferation and migration in response to high
Objective To investigate the effects of ghrelin on proliferation of vascular smooth muscle cells(VSMC)and the expression of mitochondrial fusion 2(Mfn-2)in cultured human aortic smooth muscle cells(HASMCs).Methods HASMCs were cultured in vitro,treated with different concentrations(10~(-9),10~(-8),10~(-7),10~(-6),10~(-5) mol/L)ghrelin or 10~(-6) mol/L ghrelin for different time(0,6,12,18,24h).Subconfluent HASMCs at passage 4-6were used in experiments.MTT essay was used to investigate the effect on proliferation of HASMCs.RT-PCR and Western blot were used to analyse the expression of Mfn-2.Results 10~(-7)-10~(-5) mol/L ghrelin inhibited the proliferation of HASMCs,and the inhibitory effect of concentration of 10~(-6) mol/L was the most obvious(P0.01).Ghrelin inhibited the proliferation of HASMCs in 6-24 h,and it reached the peak at 24h(P0.01).10~(-6)mol/L ghrelin significantly increased the expression of Mfn-2mRNA and protein(P0.01).The up-regulation of 10~(-6) mol/L ghrelin on Mfn-2mRNA and protein
It is well recognized that the proliferation of vascular smooth muscle cells (VSMCs) is a key event in the pathogenesis of various vascular diseases, including atherosclerosis and hypertension. It is generally considered that the phosphorylation/dephosphorylation reactions of a variety of enzymes belonging to the family of mitogen-activated protein kinases (MAPKs) play an important role in the transduction of mitogenic signal. We have previously shown that among extracellular signal-regulated protein kinases (ERKs), the 42 and 44 kDa isoforms (ERK1/2) participate in the cellular mitogenic machinery triggered by several VSMCs activators, including thrombin. ERK1/2 activation by G-protein-coupled receptors (GPCRs) has been shown to be Ca2--dependent and to require the transactivation of epidermal growth factor receptor (EGFR). In addition, it is generally admitted that variations of the intracellular Ca2- concentration ([Ca2-] i) play an important role in the transduction of mitogenic si...gnal. ...
The present method provides a method for inhibiting restenosis associated with mechanical injury of a blood vessel. Human heme oxygenase I (HO1) is directly administered at the site of injury. The present inventors have discovered that carbon monoxide generated by HO1 is involved in the molecular pathogenesis of vascular proliferative disorders. By using adenoviral-mediated expression of inducible heme oxygenase 1 in primary vascular smooth muscle cells (vsmc) in vivo, the present inventors demonstrate that in vivo expression of HO1 can be used to treat restenosis.
Smooth muscle has elongated spindle shaped cells with a single nucleus. Unlike skeletal muscle, which appears striated when stained and viewed under a light microscope, the contractile filaments in smooth muscle cells arent arranged in such an ordered, linear way. The contractile proteins are actin and myosin, the same as in skeletal muscle cells.The amount of myosin in smooth muscle cells is considerably less than in cells of skeletal muscle; the ratio of actin to myosin is about 15:1 for smooth muscle, compared to only 2:1. Smooth muscle cells are located within the walls of tubular or hollow organs or vessels for structural support. These can be divided into subtypes of smooth muscle cells; those in the vascular system, respiratory system, intestines, the eye and reproductive organs.[1] Contraction of smooth muscle is controlled by the autonomic nervous system, meaning its movements are primarily involuntary. However, as opposed to skeletal muscle, it can also be controlled by chemical and ...
Organization of cytoskeletal and myofilament elements in smooth at muscles. Diagram Of Smooth Muscle delightful to be able to the website, on this period I will teach you regarding Diagram of smooth muscle.. Now, here is the very first impression, diagram of smooth muscle, diagram of smooth muscle cells, diagram of smooth muscle tissue, diagram of smooth muscle contraction, labelled diagram of smooth muscle cell, labelled diagram of smooth muscle, histological diagram of smooth muscle, diagram of smooth cardiac and skeletal muscles :. ...
Regulator of G protein signaling 2 (RGS2), a Gq-specific GTPase activator protein (GAP), is strongly implicated in cardiovascular function. RGS2-/- mice are hypertensive and prone to heart failure and several rare human mutations that speed RGS2 degradation have been identified in hypertensive patients. Consequently, pharmacological up-regulation of RGS2 protein levels could be beneficial. We utilized a β-galactosidase complementation method to screen several thousand compounds with known pharmacological function for those that increase RGS2 protein levels. Several cardiotonic steroids (CTS), including ouabain and digoxin increase RGS2 but not RGS4 protein levels. CTS increase RGS2 protein levels through a posttranscriptional mechanism by slowing protein degradation. RGS2 mRNA levels in primary vascular smooth muscle cells are unaffected by CTS treatment while protein levels are increased 2-3 fold. Na/K-ATPase is required for the increase in RGS2 protein levels as the effect is lost in ...
Vascular calcification is the accumulation of calcium phosphate salts in the medial and intimal layers of the vessel wall and is a common complication in patients with chronic kidney disease, diabetes mellitus, and atherosclerosis.1 The earliest phase of mineralization is thought to occur via a process similar to that observed during bone formation, where chondrocytes and osteoblasts, in response to physiological signals, secrete small, specialized membrane-bound bodies termed matrix vesicles (MVs) which act to nucleate calcium phosphate (Ca/P) crystals in the form of hydroxyapatite.2-4. Editorial, see p 1281. In the vessel wall, in response to pathological signals such as inflammatory cytokines or a mineral imbalance, vascular smooth muscle cells (VSMCs) undergo osteo/chondrogenic conversion. This is characterized by expression of bone-related proteins and the release of MVs; however, the origin and mechanisms leading to release of these particles is poorly understood.4,5 Electron microscopy ...
TY - JOUR. T1 - Abnormal vascular smooth muscle cell proliferation in sural nerve biopsy from a patient with sensorimotor axonal neuropathy. AU - Luigetti, Marco. AU - Conte, Amelia. AU - Madia, Francesca. AU - Modoni, Anna. AU - Montano, Nicola. AU - Lauriola, Libero. AU - Tasca, Giorgio. AU - Del Grande, Alessandra. AU - Tonali, Pietro Attilio. AU - Sabatelli, Mario. PY - 2011/4. Y1 - 2011/4. UR - http://www.scopus.com/inward/record.url?scp=79952727942&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=79952727942&partnerID=8YFLogxK. U2 - 10.1111/j.1440-1789.2010.01179.x. DO - 10.1111/j.1440-1789.2010.01179.x. M3 - Article. C2 - 21134003. AN - SCOPUS:79952727942. VL - 31. SP - 197. EP - 198. JO - Neuropathology. JF - Neuropathology. SN - 0919-6544. IS - 2. ER - ...
TY - JOUR. T1 - Enhancement of potassium induced relaxation of isolated coronary artery smooth muscle by adenosine. AU - Foley, D. H.. AU - Mason, D. T.. AU - Amsterdam, Ezra A. PY - 1975. Y1 - 1975. N2 - Local regulation of coronary blood flow may involve an interplay of the vasoactive properties of several metabolic factors. To evaluate the effect of adenosine (Ado) on K+ induced relaxation of vascular smooth muscle, helical strips of cat coronary arteries, suspended in an organ bath of Krebs solution (37° C, 95% O2 and 5% CO2), were studied during isometric contraction stimulated by acetylcholine (ACh). From a baseline concentration of 3.0 mM, a small increment in [K+] of 2 mM induced a 16.0 ± 2.7% relaxation of tension from the initial level. However, in the presence of Ado, which induced a 20.4 ± 3.0% relaxation of 29.7 ± 4.6%. The latter was significantly greater (P , 0.005) than the response in the absence of Ado. Similarly, a 4 mM [K+] increment elicited a 14.9 ± 3.0% relaxation ...
Obesity is characterized by poor collateral vessel formation, a process involving vascular endothelial growth factor (VEGF) action on vascular smooth muscle cells (VSMC). Free fatty acids are involved in the pathogenesis of obesity vascular complications, and we have aimed to clarify whether oleic acid (OA) enhances VEGF synthesis/secretion in VSMC, and whether this effect is impaired in obesity. In cultured aortic VSMC from lean and obese Zucker rats (LZR and OZR, respectively) we measured the influence of OA on VEGF-A synthesis/secretion, signaling molecules and reactive oxygen species (ROS). In VSMC from LZR we found the following: (a) OA increases VEGF-A synthesis/secretion by a mechanism blunted by inhibitors of Akt, mTOR, ERK-1/2, PKC-beta, NADPH-oxidase and mitochondrial electron transport chain complex; (b) OA activates the above mentioned signaling pathways and increases ROS; (c) OA-induced activation of PKC-beta enhances oxidative stress, which activates signaling pathways responsible for
Obesity is characterized by poor collateral vessel formation, a process involving vascular endothelial growth factor (VEGF) action on vascular smooth muscle cells (VSMC). Free fatty acids are involved in the pathogenesis of obesity vascular complications, and we have aimed to clarify whether oleic acid (OA) enhances VEGF synthesis/secretion in VSMC, and whether this effect is impaired in obesity. In cultured aortic VSMC from lean and obese Zucker rats (LZR and OZR, respectively) we measured the influence of OA on VEGF-A synthesis/secretion, signaling molecules and reactive oxygen species (ROS). In VSMC from LZR we found the following: (a) OA increases VEGF-A synthesis/secretion by a mechanism blunted by inhibitors of Akt, mTOR, ERK-1/2, PKC-beta, NADPH-oxidase and mitochondrial electron transport chain complex; (b) OA activates the above mentioned signaling pathways and increases ROS; (c) OA-induced activation of PKC-beta enhances oxidative stress, which activates signaling pathways responsible for
Neurofibromin 2 (NF2), a potent tumor suppressor, is reported to inhibit proliferation in several cell types. The role of NF2 in neointima hyperplasia after vascular injury is unknown. We explored the role of NF2 in proliferation, migration of vascular smooth muscle cell (VSMC) and neointima hyperplasia after vascular injury. NF2 phosphorylation was elevated in VSMC subjected to platelet-derived growth factor (PDGF)-BB and in artery subjected to vascular injury. Mice deficient for Nf2 in VSMC showed enhanced neointima hyperplasia after injury, increased proliferation and migration of VSMC after PDGF-BB treatment. Mechanistically, we observed increased nuclear p-NF2, declined p-Yes-Associated Protein (YAP), nuclear translocation of YAP after PDGF-BB treatment or injury. NF2 knockdown or YAP overexpression showed similar phenotype in VSMC proliferation, migration and neointima hyperplasia. YAP inhibition abolished the above effects mediated by NF2 knockdown. Finally, NF2 knockdown further promoted
This study has investigated the influence of the vasoconstrictor peptides angiotensin II (Ang II) and endothelin-1 (ET-1) on fibronectin expression by vascular smooth muscle cells (VSMC). In confluent, quiescent cultures of VSMC, Ang II and ET-1 elevated fibronectin mRNA levels in a time- and dose-dependent fashion. ET-1 and Ang II also induced a time-dependent expression of immunoreactive fibronectin in cultures of aortic organoids, and for both peptides the fibronectin immunoreactivity was most prominent within those medial smooth muscle cell layers close to the vessel lumen. Immunoprecipitation of biosynthetically labelled fibronectin elaborated by cultured VSMC revealed a predominant expression of soluble fibronectin in response to Ang II, whereas for ET-1 the newly synthesized fibronectin was predominantly incorporated into the extracellular matrix deposit of the cells. These findings indicate that Ang II and ET-1 may exert disparate effects on smooth muscle cell phenotype and migration.
TY - JOUR. T1 - Retinoic acid-induced tissue transglutaminase and apoptosis in vascular smooth muscle cells. AU - Ou, Hesheng. AU - Haendeler, Judith. AU - Aebly, Michael R.. AU - Kelly, Louise A.. AU - Cholewa, Brian C.. AU - Koike, George. AU - Kwitek-Black, Anne. AU - Jacob, Howard J.. AU - Berk, Bradford C.. AU - Miano, Joseph M.. PY - 2000/11/10. Y1 - 2000/11/10. N2 - Retinoids exert antiproliferative and prodifferentiating effects in vascular smooth muscle cells (SMCs) and reduce neointimal mass in balloon-injured blood vessels. The mechanisms through which retinoids carry out these effects are unknown but likely involve retinoid receptor-mediated changes in gene expression. Here we report the cloning, chromosomal mapping, and biological activity of the retinoid-response gene rat tissue transglutaminase (tTG). Northern blotting studies showed that tTG is rapidly and dose-dependently induced in a protein synthesis-independent manner after stimulation with the natural retinoid all-trans ...
Mitoxantrone suppresses vascular smooth muscle cell (VSMC) proliferation and balloon injury-induced neointima formation: An in vitro and in vivo study
Recently, adipose tissue has been implicated in the regulation of vascular function in humans. This regulatory function is mediated via the release of vasoactive cytokines called adipokines. Adiponectin is an adipokine with powerful anti-inflammatory and antioxidant properties being dysregulated in obesity and in insulin resistance states. In both in vitro and in vivo models adiponectin has been shown to increase nitric oxide bioavailability, improve endothelial function, and exert beneficial effects on vascular smooth muscle cell function. Strategies to upregulate adiponectin expression or to potentiate adiponectin signalling may favourably modulate vascular redox state and therefore reduce cardiovascular risk. Various drug classes such as glitazones, newer sulfonylureas, angiotensin receptor blockers, ACE inhibitors and nicotinic acid exert beneficial effects on insulin resistance partly by increasing plasma adiponectin levels. Others such as tetrahydrobiopterin or certain antioxidants are also
Renal preglomerular arterioles regulate vascular tone to ensure a large pressure gradient over short distances, a function that is extremely important for maintaining renal microcirculation. Regulation of renal microvascular tone is impaired in salt-sensitive (SS) hypertension-induced nephropathy, but the molecular mechanisms contributing to this impairment remain elusive. Here, we assessed the contribution of the SH2 adaptor protein p66Shc (encoded by Shc1) in regulating renal vascular tone and the development of renal vascular dysfunction associated with hypertension-induced nephropathy. We generated a panel of mutant rat strains in which specific modifications of Shc1 were introduced into the Dahl SS rats. In SS rats, overexpression of p66Shc was linked to increased renal damage. Conversely, deletion of p66Shc from these rats restored the myogenic responsiveness of renal preglomerular arterioles ex vivo and promoted cellular contraction in primary vascular smooth muscle cells (SMCs) that were ...
Expression of the alpha7 integrin is developmentally regulated and is thought to be tissue-specific for both skeletal and cardiac muscles. We now report that alpha7 is also strongly and ubiquitously expressed by various types of smooth muscle, including vascular, gastrointestinal and genitourinary smooth muscles. In addition, alpha7 was surface-expressed by a number of smooth muscle cell lines that maintained their differentiated phenotype following adaptation to culture. Studies with the mouse 9E11G smooth muscle cell line showed that the alpha7 integrin mediated both adhesion and motility of these cells on laminin 1 substrates. Alpha7 expression appears to correlate with the smooth-muscle-differentiated phenotype. The multipotential P19 mouse embryonic stem cell line lacks alpha7 but uses the alpha6 integrin to adhere to laminin 1. Following retinoic acid-induced P19 differentiation predominantly to the smooth muscle cell lineage, high expression of alpha7 was detected along with partial ...
Pattie Mathieu, Paul Cahill, Joseph Mackle, James King, Caitriona Lally, Phenotypic Changes in Rat Smooth Muscle Cells Exposed to Varying Amplitudes of Cyclic Equibiaxial Tensile Strain, UK Society of Biomaterials, Belfast, Ireland, 25th-26th June 2015 ...
1) short-term dietary deficiency of magnesium (Mg; 21 days) in rats (MgD) would result in a downregulation of telomerase in cardiac and aortic smooth muscle cells, 2) low levels of Mg(2+) added to drinking water (DW) would either prevent or greatly reduce the downregulation of telomerase in MgD, 3) MgD in rats would cause an upregulation of neutral-sphingomyelinase (N-SMAse) and p53, 4) short-term MgD would result in oxidation of DNA in diverse cardiac muscle and aortic smooth muscle cells as exemplified by measurement of 8-hydroxydeoxyguanosine (8-OH-dG), and 5) cross-talk between telomerase, N-SMase, p53, and 8-OH-dG would be evident in left ventricular (LV), right ventricular (RV), atrial and aortic smooth muscle obtained from rats subjected to short-term MgD ...
Thrombomodulin (TM), a transmembrane glycoprotein highly expressed in endothelial cells (ECs), is a potent anticoagulant maintaining circulation homeostasis. Under inflammatory states, TM expression is drastically reduced in ECs while vascular smooth muscle cells (VSMCs) show a robust expression of TM. The functional role of TM in VSMCs remains elusive. We examined the role of TM in VSMCs activities in human aortic VSMCs stimulated with platelet-derived growth factor-BB (PDGF-BB). Using rat embryonic aorta-derived A7r5 VSMCs which do not express TM, the role of the chondroitin sulfate (CS) moiety of TM in VSMCs was delineated with cells expressing wild-type TM and the CS-devoid TM mutant. Expression of TM enhanced cell migration and adhesion/spreading onto type I collagen, but had no effect on cell proliferation. Knocking down TM with short hairpin RNA reduced PDGF-stimulated adhesion and migration of human aortic VSMCs. In A7r5 cells, TM-mediated cell adhesion was eradicated by pretreatment with
A number of studies have asserted that moderate drinking has a positive benefit on cardiovascular health. Now, scientists at the University of Rochester Medical Center have discovered how alcohol consumption can help to prevent heart disease. The research, published in the journal Arteriosclerosis, Thrombosis and Vascular Biology, studied the effects of moderate amounts of alcohol in human coronary artery smooth muscle cells and in the carotid arteries of mice [1]. In both cases, regular, limited amounts of alcohol inhibited a protein called Notch 1 and prevented the buildup of smooth muscle cells in blood vessels that leads to the narrowing of the arteries and can put you at risk for a heart attack or stroke.. ...
To generate temporally-controlled targeted somatic mutations selectively and efficiently in smooth muscles, we have established a transgenic SMA-Cre-ER(T2) mouse line in which the expression of the Tamoxifen-dependent Cre-ER(T2) recombinase is under the control of a large genomic DNA segment of the mouse smooth muscle alpha actin (SMA) gene, contained in a Bacterial artificial chromosome (Bac). In this transgenic mouse line, Cre-ER(T2)-mediated recombination of LoxP-flanked target DNA is strictly Tamoxifen-dependent, and efficient in both vascular and visceral smooth muscle cells. Moreover, with the exception of few cardiomyocytes, LoxP-flanked DNA excision is restricted to smooth muscle cells. Thus, SMA-Cre-ER(T2) mice should be of great value to analyze gene function in smooth muscles, and to establish new animal models of human smooth muscle disorders.
This study was conducted to determine the interaction of individual corrosion products from biodegradable iron stents with cells from the adjacent tissue. The response of human umbilical venous smooth muscle cells (SMCs) to an excess of ferrous ions was investigated in a cell culture model at the phenotypic and at the molecular level. When soluble ferrous ions were added to the cell culture medium the cell growth rate was reduced. Gene expression profiling indicated a reduction in the amounts of mRNA from genes that are required for cell proliferation. In addition, mRNA was regulated from multiple genes involved in iron homeostasis, DNA replication and lipid metabolism. In conclusion, ions released from iron stents could reduce the vascular SMC proliferation rate by influencing growth-related gene expression and may therefore play a beneficial role in antagonizing restenosis in vivo. ...
BioAssay record AID 568587 submitted by ChEMBL: Vasodilatory activity in Sprague-Dawley rat thoracic aorta smooth muscle assessed as inhibition of phenylephrine-induced vasoconstriction.
Vascular smooth muscle cells (SMCs) populate in the media of the blood vessel, and play an important role in the control of vasoactivity and the remodeling of the vessel wall. Blood vessels are constantly subjected to hemodynamic stresses, and the pulsatile nature of the blood flow results in a cyclic mechanical strain in the vessel walls. Accumulating evidence in the past two decades indicates that mechanical strain regulates vascular SMC phenotype, function and matrix remodeling. Bone marrow mesenchymal stem cell (MSC) is a potential cell source for vascular regeneration therapy, and may be used to generate SMCs to construct tissue-engineered vascular grafts for blood vessel replacements. In this review, we will focus on the effects of mechanical strain on SMCs and MSCs, e.g., cell phenotype, cell morphology, cytoskeleton organization, gene expression, signal transduction and receptor activation. We will compare the responses of SMCs and MSCs to equiaxial strain, uniaxial strain and mechanical strain
Definition of smooth muscle cell in the Financial Dictionary - by Free online English dictionary and encyclopedia. What is smooth muscle cell? Meaning of smooth muscle cell as a finance term. What does smooth muscle cell mean in finance?
Smooth muscle fibers are spindle-shaped, and, like all muscle, can contract and relax. In the relaxed state, each cell is spindle-shaped, 20-500 micrometers long, and 5 micrometers wide.[1] There are two types of smooth muscle arrangements in the body: multi-unit and single-unit. The single-unit type, also called unitary smooth muscle, is far more common. Whereas the former presents itself as distinct muscle fibers that are usually activated by their own nerve fibers, the latter operate as a single unit and are arranged in sheets or bundles. Unitary smooth muscle is also commonly referred to as visceral smooth muscle because it is found in the walls of the viscera, or internal organs, of the body, including the intestines, ducts such as the bile ducts, ureters and oviducts, and most blood vessels.[2] Unitary smooth muscle can be further divided into phasic and tonic. The cells that compose smooth muscle have, in general, single nuclei. The cells are arranged in sheets or bundles and connected by ...
Human Umbilical Vein Smooth Muscle Cell Pellet https://www.sciencepro.com.br/produtos/sc-cp8020 https://www.sciencepro.com.br/@@site-logo/logo-novo.png ...
Apelin receptor upregulation in spontaneously hypertensive rat contributes to the enhanced vascular smooth muscle cell proliferation by activating autophagy
Introduction Aberrant sensing and transmission of force by vascular smooth muscle cells (VSMC) results in vascular remodelling, increased arterial stiffness and hypertension. Actin cytoskeleton (CK) remodelling is essential for VSMC responses to vasoconstrictors and mechanical stimuli. Focal adhesions (FAs) link the extracellular matrix and the actin CK allowing sensing and transmission of force. Hic-5 is highly expressed in VSMC and regulates FA assembly and actin CK remodelling in arteries.. ...
vascular permeability; vascular smooth muscle contraction; allergy. antagonists of CYSLTR1 used in asthma as well as other ... vascular permeability; vascular smooth muscle contraction; allergy. antagonists of CYSLTR1 used in asthma as well as other ... platelet aggregation, vascular smooth muscle contraction. PGI2 analogs used to treat vascular disorders like pulmonary ... They stimulate vascular permeability in an ex vivo human vascular endothelial model system,[87] and in a small study of 32 ...
Takahashi K, Hiwada K, Kokubu T (June 1988). "Vascular smooth muscle calponin. A novel troponin T-like protein". Hypertension. ... Winder SJ, Walsh MP (June 1990). "Smooth muscle calponin. Inhibition of actomyosin MgATPase and regulation by phosphorylation ... "Entrez Gene: ACTA1 actin, alpha 1, skeletal muscle". Bandman E (December 1992). "Contractile protein isoforms in muscle ... "Alpha-skeletal actin induces a subset of muscle genes independently of muscle differentiation and withdrawal from the cell ...
... smooth-muscle relaxants and vasodilators, injected into the penis; penile implants; penis pumps; and vascular reconstructive ... which causes the relaxation of the smooth muscles of the corpora cavernosa (the main erectile tissue of the penis), and ... and the mechanism of action was clearly corporal smooth muscle relaxation. The effect that Brindley discovered established the ... Vascular reconstructive surgeries are beneficial in certain groups. Treatments, other than surgery, do not fix the underlying ...
On vascular smooth muscle cells if not otherwise specified Transduction (↑ = increases. ↓ = decreases)[5] ... within vascular smooth muscle cells.[2] However, the specific mechanisms for generating an increased intracellular ... On smooth muscle cells: Activation of Gq --, ↑PLC activity --, ↑IP3 and DAG --, activation of IP3 receptor in SR --, ↑ ... Arginine vasopressin receptor 1 (V1) on smooth muscle cells Activation of Gq --, ↑PLC activity --, ↑IP3 and DAG --, activation ...
Matsumoto T, Kobayashi T, Kamata K (August 2003). "Phosphodiesterases in the vascular system". J Smooth Muscle Res. 39 (4): 67- ... PDE1C has been shown to be a major regulator of smooth muscle proliferation, at least in human smooth muscle. Nonproliferating ... PDE1A most likely serves to regulate vascular smooth muscle concentration and has been found to be up-regulated in rat aorta in ... For example, in airway smooth muscles of humans and other species, generic PDE1 accounts for more than 50% of the hydrolytic ...
"Expression of functional delta opioid receptors in vascular smooth muscle". International Journal of Molecular Medicine. 6 (6 ...
"The pharmacology of vascular smooth muscle". Pharmacological Reviews. 7 (2): 184-265, hier S. 213. PMID 13245382. S. Guimarães ... und β-adrenoceptors co-existing in vascular smooth muscle. Veins and their receptors remained favourites. Guimarães has ... S. Guimarães, I. Azevedo, W. Cardoso, M. C. Oliveira (1975). "Relation between the amount of smooth muscle of venous tissue and ... In 1982, Guimarães wrote in Trends in Pharmacological Sciences: „In vascular tissue there are two different biophases for ...
Szasz, Theodora; Tostes, Rita C. A. (2016). Vascular Smooth Muscle Function in Hypertension. Biota Publishing. ISBN ... muscles, nerves, veins and arteries; and special anatomy which is concerned with the internal parts of the body like the heart ...
Calcification forms among vascular smooth muscle cells of the surrounding muscular layer, specifically in the muscle cells ... of plaque-resident cells are vascular smooth muscle cell derived. Therefore, it is important to research the role of vascular ... Vascular smooth muscle cells play a key role in atherogenesis and were historically considered to be beneficial for plaque ... However, in addition to the fibrous cap, vascular smooth muscle cells also give rise to many of the cell types found within the ...
... vascular endothelial and smooth muscle cells; various types of epithelial cells, liver hepatocytes, neural tissue glial cells, ...
Khalil, Raouf A. (2010). Rho Kinase in Vascular Smooth Muscle. Morgan & Claypool Life Sciences. Nagumo, Hiromitsu; Sasaki, ... On a cellular level, ROCK has multiple functions, including regulation of smooth muscle cell contraction, cell migration, and ... "RhoA/ROCK Pathway Activation is Regulated by AT1 Receptor and Participates in Smooth Muscle Migration and Dedifferentiation via ... "Rho kinase inhibitor HA-1077 prevents Rho-mediated myosin phosphatase inhibition in smooth muscle cells". American Journal of ...
PKG reduces intracellular Ca2+ in vascular smooth muscle to increase smooth muscle relaxation and promote blood flow. PKG also ... "Cyclic GMP-dependent protein kinase regulates vascular smooth muscle cell phenotype". Journal of Vascular Research. 34 (4): 245 ... "cGMP-dependent protein kinase mediates the reduction of Ca2+ by cAMP in vascular smooth muscle cells". American Journal of ... decreased accumulation of ROS lowers oxidative stress in vascular smooth muscle cells, decreasing oxidative degeneration of BH4 ...
PKG reduces intracellular Ca2+ in vascular smooth muscle to increase smooth muscle relaxation and promote blood flow. PKG also ... "Cyclic GMP-dependent protein kinase regulates vascular smooth muscle cell phenotype". Journal of Vascular Research. 34 (4): 245 ... Nitric oxide (NO) contributes to vessel homeostasis by inhibiting vascular smooth muscle contraction and growth, platelet ... "cGMP-dependent protein kinase mediates the reduction of Ca2+ by cAMP in vascular smooth muscle cells". American Journal of ...
Jan 2016). "MFAP4 Promotes Vascular Smooth Muscle Migration, Proliferation and Accelerates Neointima Formation". ... expression levels of MFAP4 correlate with alterations in extracellular matrix genes within human aortic vascular smooth muscle ... Sep 2015). "Microfibrillar-associated Protein 4 Modulates Airway Smooth Muscle Cell Phenotype in Experimental Asthma". Thorax. ... Journal of Vascular Surgery. 71 (6): 1921-1929. doi:10.1016/j.jvs.2019.08.253. PMID 31784280. Wulf-Johansson, et al. (Dec 2013 ...
... adrenoceptors in human vascular smooth muscle cells". American Journal of Physiology. Heart and Circulatory Physiology. 286 (1 ...
Hagiwara M, Endo T, Hidaka H (February 1984). "Effects of vinpocetine on cyclic nucleotide metabolism in vascular smooth muscle ... and vascular cell adhesion molecule-1 (VCAM-1). In mice, vinpocetine reduced lipopolysaccharide inoculation induced ...
... which reach vascular smooth muscle. The vasomotor center changes vascular smooth muscle tone. This changes local and systemic ... This reduces sympathetic tone to vascular smooth muscle. This reduces heart rate and vascular resistance. Digoxin increases ...
"Chapter 7Rho Kinase in Vascular Smooth Muscle". Jacobs M, Hayakawa K, Swenson L, Bellon S, Fleming M, Taslimi P, Doran J ( ... Other functions involve smooth muscle contraction, actin cytoskeleton organization, stress fiber and focal adhesion formation, ... "Rho-associated kinase of chicken gizzard smooth muscle". The Journal of Biological Chemistry. 274 (6): 3744-52. doi:10.1074/jbc ... Fasudil has been used to characterize the role of ROCK1 in vascular function in clinical studies and has been approved for use ...
Robinson, B. F. (1981). "Drugs acting directly on vascular smooth muscle". British Journal of Clinical Pharmacology. 12 (Suppl ... Vallance, Patrick (1997). "Exploring vascular nitric oxide in health and disease. The Goulstonian Lecture 1996". Journal of the ...
"Vascular smooth muscle contractility depends on cell shape". Integrative Biology. 3 (11): 1063-70. doi:10.1039/c1ib00061f. PMID ... Walboomers, X. F.; Monaghan, W.; Curtis, A. S. G.; Jansen, J. A. (August 1999). "Attachment of fibroblasts on smooth and ...
They mainly control smooth and vascular muscle dilation. Strength of response is dependent upon the concentration of receptors ...
"Protein Kinase C as Regulator of Vascular Smooth Muscle Function and Potential Target in Vascular Disorders". Vascular ... Since smooth muscle does not contain a troponin complex, as striated muscle does, this mechanism is the main pathway for ... Another source of smooth muscle disorders like ischemia-reperfusion, hypertension, and coronary artery disease arise when ... Four different MYLK isoforms exist: MYLK1 - smooth muscle MYLK2 - skeletal MYLK3 - cardiac MYLK4 - novel These enzymes are ...
"CCN3 inhibits neointimal hyperplasia through modulation of smooth muscle cell growth and migration". Arteriosclerosis, ... However, Nov-null mice show enhanced blood vessel neointimal thickening when challenged with vascular injury, indicating that ... Journal of Vascular Research. 40 (3): 234-43. doi:10.1159/000071887. PMID 12902636. S2CID 84511515. Lin CG, Chen CC, Leu SJ, ... Thrombosis, and Vascular Biology. 30 (4): 675-82. doi:10.1161/ATVBAHA.110.203356. PMID 20139355. Bleau AM, Planque N, Lazar N, ...
Jiang Y, Yin H, Zheng XL (November 2010). "MicroRNA-1 inhibits myocardin-induced contractility of human vascular smooth muscle ... as its loss of function resulted in a reduction in smooth muscle cell biomarkers and a reduction in the derived smooth muscle ... There is evidence that the control of smooth muscle cell differentiation by MiR-1 may be mediated by the down regulation of ... MiR-1 has key roles in the development and differentiation of smooth and skeletal muscles. For example, in the lineage-specific ...
"Isolation of multiple types of plasminogen activator inhibitors from vascular smooth muscle cells". Thrombosis and Haemostasis ... "Serpins promote cancer cell survival and vascular co-option in brain metastasis". Cell. 156 (5): 1002-16. doi:10.1016/j.cell. ... "Imaging of Angiotropism/Vascular Co-Option in a Murine Model of Brain Melanoma: Implications for Melanoma Progression along ...
"Role of the small heat shock proteins in regulating vascular smooth muscle tone". Journal of the American College of Surgeons. ... Hsp20 phosphorylation correlates well with smooth muscle relaxation and is one significant phosphoprotein involved in the ... "Small heat shock proteins in smooth muscle". Pharmacology & Therapeutics. 119 (1): 44-54. doi:10.1016/j.pharmthera.2008.04.005 ... Hsp20 appears significant in development of the smooth muscle phenotype during development. Hsp20 also serves a significant ...
Atherosclerotic plaque contains vascular smooth muscle cells, macrophages and endothelial cells and these have been found to ... Uryga AK, Bennett MR (15 April 2016). "Ageing induced vascular smooth muscle cell senescence in atherosclerosis". J Physiol. ... Muscle strength, and stamina for sustained physical effort, decline in function with age in humans and other species. Skeletal ... reported that the oxidative DNA damage 8-OHdG accumulates in heart and skeletal muscle (as well as in brain, kidney and liver) ...
"Vascular smooth muscle cell proliferation as a therapeutic target. Part 2: Natural products inhibiting proliferation". ... The drug is mainly to inhibit neointimal growth (due to the proliferation of smooth muscle cells) that would cause restenosis. ... Macrophages accumulate around the stent, and nearby smooth muscle cells proliferate. These physiological changes, which can ... Finn AV, Nakazawa G, Joner M, Kolodgie FD, Mont EK, Gold HK, Virmani R (2007). "Vascular responses to drug eluting stents: ...
... vascular smooth muscle and gastric fundus mucosal cells); thalamus (anterior, ventromedial, laterodorsal, paraventricular and ... This effect was associated with a reduction in the levels of Vascular endothelial growth factor and matrix metalloproteinase-9 ... Activation of EP3 receptors contracts vascular beds including rat mesentery artery, rat tail artery, guinea-pig aorta, rodent ...
... refers to proliferation and migration of vascular smooth muscle cells primarily in the tunica intima, ... Macrophages in particular express many growth factors, cytokines, and enzymes that facilitate vascular smooth muscle cell ... "Vascular smooth muscle cell proliferation as a therapeutic target. Part 1: Molecular targets and pathways". Biotechnology ... proliferation and migration of vascular smooth muscle cells, and collagen deposition. Mechanical injury of arterials due to ...
One of the main advantages of using PET is that it can also provide muscle activation data about deeper lying muscles such as ... Cardiology, atherosclerosis and vascular disease study: In clinical cardiology, FDG-PET can identify so-called "hibernating ... a smoothing prior leading to total variation regularization or a Laplacian distribution leading to ℓ. 1. {\displaystyle \ell _{ ... Musculoskeletal imaging: PET has been shown to be a feasible technique for studying skeletal muscles during exercises like ...
"Muscle Activation of Paraspinal Muscles in Different Types of High Heels during Standing." Journal of Physical Therapy Science ... Lastly, American Smooth shoes are closed toed, flexible soled shoes that range in heel height from 2 to 2.5 inches. An ... "Influence of High-Heeled Shoes on Venous Function in Young Women." Journal of Vascular Surgery, vol. 56, Oct 2012. ... The researchers mentioned that over time these results would increase local muscle fatigue that could lead to muscle swelling, ...
Smooth. muscle. *Calmodulin. *Vascular smooth muscle. Striated. muscle. Skeletal. muscle. Costamere/. DAPC. ... Muscle spindles are stretch receptors within the body of a muscle that primarily detect changes in the length of the muscle. ... Muscle spindles are found within the belly of muscles, between extrafusal muscle fibers.[b] The specialised fibers that ... Muscle spindle. Mammalian muscle spindle showing typical position in a muscle (left), neuronal connections in spinal cord ( ...
... such as the effects of inflammatory mediators on airway and vascular smooth muscle tone. As a rule of thumb, all these models ... Histological changes consist of epithelial necrosis and detachment, increase in the area of smooth muscle, epithelial ... is affected by increases in the dispersion of both alveolar ventilation and cardiac output because bronchial and vascular ...
a) Vascular thrombosis in three or more organs or tissues and. *b) Development of manifestations simultaneously or in less than ... Anti-smooth muscle *Anti-actin. *Anti-TPO/Antimicrosomal. Cell membrane. *Anti-ganglioside ... Classification with APS requires evidence of both one or more specific, documented clinical events (either a vascular ... are associated with thrombosis and vascular disease. The syndrome can be divided into primary (no underlying disease state) and ...
Julie Hazel Campbell is a cell biologist specializing in vascular smooth muscle. Dr. Campbell's postdoctoral experiences ... vascular smooth muscle and tissue engineering of the arteries. - Therapeutic Uses of Beta-casein a2 and dietary supplement ... Her studies consolidated her early findings on vascular smooth muscle biology. In 1991, she left her position as the Principal ... In the early 1970s, she was the first to discover that smooth muscle cells can exist in a spectrum of phenotypes that control ...
Congenital smooth muscle hamartoma. *Cystic lymphatic malformation. *Median raphe cyst. *Melanotic neuroectodermal tumor of ...
... reach underlying vascular smooth muscle cells at a concentration sufficient to activate ion channels, and initiate smooth ... its action is to hyperpolarize vascular smooth muscle cells, causing these cells to relax, thus allowing the blood vessel to ... Contact-mediated mechanisms bestow endothelial hyperpolarization that passively spreads to the smooth muscle through inter- ... "Endothelium-dependent smooth muscle hyperpolarization: do gap junctions provide a unifying hypothesis?". British Journal of ...
... vascular smooth muscle cells and mesenchymal stem cells as well as chemotaxis, the directed migration, of mesenchymal cells. ... PDGF[1][2] is a potent mitogen for cells of mesenchymal origin, including fibroblasts, smooth muscle cells and glial cells. In ... it is also produced by other cells including smooth muscle cells, activated macrophages, and endothelial cells[5] ... Other growth factors in this family include vascular endothelial growth factors B and C (VEGF-B, VEGF-C)[16][17] which are ...
It also causes contraction of non-vascular smooth muscle in the bronchus and gut, increases vascular permeability and is also ... from the effect of snake venom on intestinal smooth muscle, which was noted to slowly contract.[citation needed] ...
positive regulation of vascular smooth muscle cell proliferation. • negative regulation of gene expression. • protein ... positive regulation of smooth muscle cell proliferation. • positive regulation of protein kinase activity. • positive ... positive regulation of leukocyte adhesion to vascular endothelial cell. • positive regulation of blood microparticle formation ... "The diseasome of physical inactivity - and the role of myokines in muscle-fat cross talk". J Physiol. 587 (23): 5559-5568. doi ...
There is a smooth muscle layer below the epithelium arranged as two ribbons of muscle that spiral in opposite directions. This ... "Journal of Cardiothoracic and Vascular Anesthesia. 17 (3): 289-98. doi:10.1016/S1053-0770(03)00046-6. PMID 12827573. Archived ... Hyaline cartilage is present in the bronchi, surrounding the smooth muscle layer. In the main bronchi, the cartilage forms C- ... As the cartilage decreases, the amount of smooth muscle increases. The mucous membrane also undergoes a transition from ...
Underlying the mucous membrane in the mouth is a thin layer of smooth muscle tissue and the loose connection to the membrane ... Vascular *Budd-Chiari syndrome. *Hepatic veno-occlusive disease. *Portal hypertension. *Nutmeg liver ... The muscular layer of the body is of smooth muscle tissue that helps the gallbladder contract, so that it can discharge its ... The suspensory muscle attaches the ascending duodenum to the diaphragm. This muscle is thought to be of help in the digestive ...
Some of the other signs are poor eyelid function, contracture of the facial muscles, a backward tilt of the head with ... These are fine movements, that can be mistaken for nystagmus, except that they are saccadic in nature, with no smooth phase. ... strength training with progressive resistive exercises and isokinetic exercises and stretching of the neck muscles.[37] While ... stiffening of the neck muscles, sleep disruption, urinary incontinence and constipation. The visual symptoms are of particular ...
Nicotine exposure alters human vascular smooth muscle cell phenotype from a contractile to a synthetic type. Atherosclerosis ...
... which relax smooth muscle of constricted airway in asthma, or (4) mast cell stabilizers, which inhibit the degranulation of ... and increased vascular permeability, it is presumed, to allow other immune cells to gain access to tissues, but which can lead ...
The common ostrich's sternum is flat, lacking the keel to which wing muscles attach in flying birds.[17] The beak is flat and ... The feathers lack the tiny hooks that lock together the smooth external feathers of flying birds, and so are soft and fluffy ... The air then flows through the anatomical dead space of a highly vascular trachea (c. 78 cm (31 in)) and expansive bronchial ... During expiration, oxygen poor air flows to the anterior air sacs[62] and is expelled by the action of the expiratory muscles. ...
It increases vessel permeability, dilates blood vessels and causes smooth muscle cells to contract. Bradykinin plays an ... "Vascular Health and Risk Management. 6: 795-802. doi:10.2147/vhrm.s4332. PMC 2941790. PMID 20859548.. ...
Congenital smooth muscle hamartoma. *Cystic lymphatic malformation. *Median raphe cyst. *Melanotic neuroectodermal tumor of ...
... induces iNOS in bovine vascular smooth muscle cells: no relationship between nitric oxide production and gamma-carboxylation ...
They are the superior longitudinal muscle, the inferior longitudinal muscle, the vertical muscle, and the transverse muscle. ... A deceptive person is said to have a forked tongue, and a smooth-talking person said to have a silver tongue. ... The sublingual route takes advantage of the highly vascular quality of the oral cavity, and allows for the speedy application ... MusclesEdit. The eight muscles of the human tongue are classified as either intrinsic or extrinsic. The four intrinsic muscles ...
... and LTE4 which promote vascular permeability, contract airways smooth muscle, and otherwise perturb these tissues and b) LTB4 ... monoxime exerts a dual mode of inhibition towards leukotriene-mediated vascular smooth muscle cell migration". Cardiovascular ... Fibroblasts, smooth muscle cells and endothelial cells express low levels of ALOX5.[6][7] Up-regulation of ALOX5 may occur ... micro-vascular permeability, and mucus secretion; they likewise contribute to various allergic and non-allergic reactions ...
negative regulation of vascular smooth muscle cell proliferation. Sources:Amigo / QuickGO. Orthologs. ...
Azzopardi G.; Petkov N. (2011). Detection of retinal vascular bifurcations by trainable V4-like filters, in Computer Analysis ... The mapping of vascular bifurcations is one of the basic steps in biometric identification.[45] Results of such analyses of ... "Retinal fundus images - Ground truth of vascular bifurcations and crossovers". University of Groningen. Retrieved 20 April 2018 ... In birds, the pecten is a vascular structure of complex shape that projects from the retina into the vitreous humour; it ...
Congenital smooth muscle hamartoma. *Cystic lymphatic malformation. *Median raphe cyst. *Melanotic neuroectodermal tumor of ...
The water vascular system that develops from their middle coelom or hydrocoel. Echinoderms use this system for many things ... In recent years, the sea cucumber industry in Alaska has increased due to increased demand for the skins and muscles to China.[ ... the podia can be of smooth aspect or provided with fleshy appendages (like Thelenota ananas). The podia on the dorsal surface ... In most sea cucumbers, this is the only substantial part of the skeleton, and it forms the point of attachment for muscles that ...
Smooth. muscle. *Calmodulin. *Vascular smooth muscle. Striated. muscle. Skeletal. muscle. Costamere/. DAPC. ... This muscle article is a stub. You can help Wikipedia by expanding it.. *v ... Perimysium is a sheath of connective tissue that groups muscle fibers into bundles (anywhere between 10 and 100 or more) or ... Studies of muscle physiology suggest that the perimysium plays a role in transmitting lateral contractile movements. This ...
smooth muscle:. *Leiomyoma/leiomyosarcoma. skeletal muscle:. *Rhabdomyoma/rhabdomyosarcoma: Embryonal rhabdomyosarcoma *Sarcoma ... vascular. *see Template:Soft tissue tumors and sarcomas, Template:Vascular tumors, Template:Myeloid malignancy (for ...
By acting on vascular smooth muscle, they reduce contraction of the arteries and cause an increase in arterial diameter, a ... The class of CCBs known as dihydropyridines mainly affect arterial vascular smooth muscle and lower blood pressure by causing ... CCBs do not work on venous smooth muscle).. *By acting on cardiac muscles (myocardium), they reduce the force of contraction of ... Voltage-dependent calcium channels are responsible for excitation-contraction coupling of skeletal, smooth, and cardiac muscle ...
... smooth muscle and the extracellular matrix are quantitatively the largest components of the aortic vascular wall. The ... This contribution of the neural crest to the great artery smooth muscle is unusual as most smooth muscle is derived from ... The smooth muscle of the great arteries and the population of cells that form the aorticopulmonary septum that separates the ... In fact the smooth muscle within the abdominal aorta is derived from mesoderm, and the coronary arteries, which arise just ...
Purchase Vascular Smooth Muscle: Metabolic, Ionic, and Contractile Mechanisms - 1st Edition. Print Book & E-Book. ISBN ... Vascular Smooth Muscle: Metabolic, Ionic, and Contractile Mechanisms addresses the vascular smooth muscle function by ... Vascular Smooth Muscle: Metabolic, Ionic, and Contractile Mechanisms 1st Edition. 0 star rating Write a review ... 1. Vascular Smooth Muscle: Relations between Energy Metabolism and Mechanics. I. Introduction. II. Relations between Metabolism ...
Abnormal vascular smooth muscle cell (SMC) proliferation and migration contribute to the development of restenosis after ...
... Nahed El-Najjar, Rashmi P. Kulkarni, Nancy Nader, Rawad ... "Effects of Hyperglycemia on Vascular Smooth Muscle Ca2+ Signaling," BioMed Research International, vol. 2017, Article ID ...
... Nahed El-Najjar, Rashmi P. Kulkarni, Nancy Nader, Rawad ... J.-B. Roullet, K.-H. Le Quan Sang, U. Luft et al., "Inhibition of Ca2+ uptake into A7r5 vascular smooth muscle cells by ... K. D. Wu, D. Bungard, and J. Lytton, "Regulation of SERCA Ca2+ pump expression by cytoplasmic Ca2+ in vascular smooth muscle ... P. L. Faries, D. I. Rohan, H. Takahara et al., "Human vascular smooth muscle cells of diabetic origin exhibit increased ...
... smooth muscle endothelial and nerve) level through to the blood vessel wall to the vascular system as a functional system. This ... and is a source of background literature for research in vascular pharmacology. ... The Pharmacology of Vascular Smooth Muscle. C. J. Garland and J. A. Angus. Abstract. This book provides an understanding of how ... Regulation of vascular smooth muscle tone in sepsis Richard G. Bogle, and Patrick Vallance. ...
... smooth, vascular"[MeSH Terms] OR ("muscle"[All Fields] AND "smooth"[All Fields] AND "vascular"[All Fields]) OR "vascular smooth ... Adeno-associated virus vector transduction of vascular smooth muscle cells in vivo. Richter M et al. Physiol Genomics. (2000) ... Adeno-associated virus vector transduction of vascular smooth muscle cells in vivo. ... muscle"[All Fields] OR ("vascular"[All Fields] AND "smooth"[All Fields] AND "muscle"[All Fields])) AND ("cells"[MeSH Terms] OR ...
We tested the hypothesis that IL-10 may also inhibit vascular sm... ... IL-10 inhibits vascular smooth muscle cell activation in vitro and in vivo.. *Mazighi M ... We tested the hypothesis that IL-10 may also inhibit vascular smooth muscle cell (SMC) activation via the inhibition of the NF- ...
Vascular smooth muscle contraction [ Pathway menu , Organism menu , Pathway entry , Download KGML , Show description , User ... The vascular smooth muscle cell (VSMC) is a highly specialized cell whose principal function is contraction. On contraction, ...
They are increasingly used to monitor the smooth muscle cell differentiation process to a contractile or synthetic phenotype. ... B have only been found in fully differentiated contractile smooth muscle cells. ... Muscle Contraction / physiology*. Muscle Proteins / physiology*. Muscle, Smooth, Vascular / physiology*. Myocytes, Smooth ... Vascular-specific smoothelin-B is the first smooth muscle cell marker that disappears when vascular tissues are compromised, ...
5 Abstracts with Vascular smooth muscle cell (VSMC) inhibitor Research. Filter by Study Type. In Vitro Study. ... Honokiol inhibits vascular smooth muscle cell proliferation, indicating it may have a role in arteriosclerosis treatment. Apr ... 7 Substances Researched for Vascular smooth muscle cell (VSMC) inhibitor Name. AC. CK. Focus. ... Pharmacological Actions : Antioxidants, Antiproliferative , Nitric Oxide Enhancer, Vascular smooth muscle cell (VSMC) inhibitor ...
Vascular smooth muscle cells (SMCs) and pericytes are essential for the stabilisation of nascent immature endothelial tubes. ... Human embryonic stem cell-derived vascular smooth muscle cells in therapeutic neovascularisation.. Cheung C1, Sinha S. ... We then summarise the methods of derivation of smooth muscle progenitors and cells from human ESCs. The primary emphasis is on ... This review begins with developmental insights into a range of smooth muscle progenitors from studies on embryos and ESC ...
SGK1 induces vascular smooth muscle cell calcification through NF-κB signaling. ... SGK1 induces vascular smooth muscle cell calcification through NF-κB signaling. ... chondrogenic transdifferentiation of vascular smooth muscle cells (VSMCs). Here, we describe that serum- and glucocorticoid- ... Treatment of human aortic smooth muscle cells with serum from uremic patients induced osteo-/chondrogenic transdifferentiation ...
Aortic vascular smooth muscle cells (vascular smooth muscle cells [VSMCs]) were isolated from Sprague-Dawley rats as described ... Rapid effects of aldosterone on clonal human vascular smooth muscle cells. Am J Physiol Cell Physiol. 2007; 292: C788-C794. ... Biosynthesis and a link to angiotensin II-induced hypertrophy of vascular smooth muscle cells. J Biol Chem. 1994; 269: 24316- ... Glucocorticoid-Related Signaling Effects in Vascular Smooth Muscle Cells. Gergö A. Molnar, Carsten Lindschau, Galyna Dubrovska ...
... a novel troponin T-like protein was purified from bovine aorta smooth muscle. The isolated protein was separated into several ... In a search for additional Ca2+ regulatory components in vascular smooth muscle, ... Vascular smooth muscle calponin. A novel troponin T-like protein Hypertension. 1988 Jun;11(6 Pt 2):620-6. doi: 10.1161/01.hyp. ... In a search for additional Ca2+ regulatory components in vascular smooth muscle, a novel troponin T-like protein was purified ...
Nanoscale coupling of junctophilin-2 and ryanodine receptors regulates vascular smooth muscle cell contractility. Harry A. T. ... Nanoscale coupling of junctophilin-2 and ryanodine receptors regulates vascular smooth muscle cell contractility ... Nanoscale coupling of junctophilin-2 and ryanodine receptors regulates vascular smooth muscle cell contractility ... Nanoscale coupling of junctophilin-2 and ryanodine receptors regulates vascular smooth muscle cell contractility ...
Vascular smooth muscle possesses all of the properties of a rhythmic system (3). Spontaneous, rhythmic contractions of blood ... Slow Oscillations of Transmembrane Na und K Fluxes in Vascular Smooth Muscle. In: Betz E. (eds) Vascular Smooth Muscle / Der ... Oscillating fluxes and membrane potentials in vascular smooth muscle and cardiac muscle. Pflügers Arch. ges. Physiol, (in ... Vascular smooth muscle possesses all of the properties of a rhythmic system (3). Spontaneous, rhythmic contractions of blood ...
Impairment of vascular smooth muscle cells (VSMC) is recognized as a predisposition factor for atherosclerosis development. We ... to metabolic alterations may alter the physiology of VSMC and thus accelerate the development of metabolic-related vascular ... Impairment of vascular smooth muscle cells (VSMC) is recognized as a predisposition factor for atherosclerosis development. We ... El Akoum, S., Cloutier, I. and Tanguay, J.F. (2011) Vascular smooth muscle cell alterations triggered by mice adipocytes: Role ...
... suggesting that NO affects vascular remodeling during restenosis via alternative mechanisms. ... Role of smooth muscle cGMP/cGKI signaling in murine vascular restenosis Arterioscler Thromb Vasc Biol. 2008 Jul;28(7):1244-50. ... is of crucial importance for smooth muscle cell (SMC) function and exerts numerous, and sometimes opposing, effects on vascular ... The purpose of this study was to examine the functional role of the smooth muscle cGMP/cGKI signaling cascade in restenosis of ...
Vascular smooth muscle contraction - Homo sapiens (human) [ Pathway menu , Organism menu , Pathway entry , Download KGML , Show ... The vascular smooth muscle cell (VSMC) is a highly specialized cell whose principal function is contraction. On contraction, ...
Vascular smooth muscle refers to the particular type of smooth muscle found within, and composing the majority of the wall of ... The adrenergic receptors exert opposite physiologic effects in the vascular smooth muscle under activation: *α1 receptors. ... Vascular smooth muscle contracts or relaxes to both change the volume of blood vessels and the local blood pressure, a ... Vascular smooth muscle is innervated primarily by the sympathetic nervous system through adrenergic receptors (adrenoceptors). ...
vascular smooth muscle cells;. WT,. wild type;. BAC,. bacterial artificial chromosome;. PG,. proteoglycan;. NP,. sodium ... Progressive vascular smooth muscle cell defects in a mouse model of Hutchinson-Gilford progeria syndrome. Renee Varga, Maria ... Smooth muscle α-actin staining confirms loss of VSMCs; these images also show the eccentric distribution of vascular damage, ... These mice develop progressive loss of vascular smooth muscle cells in the medial layer of large arteries, in a pattern very ...
Na+, K(+)-adenosine triphosphatase regulation in hypertrophied vascular smooth muscle cells.. L M Krug, B C Berk ... Vascular smooth muscle cell hypertrophy is a normal compensatory state that may play a pathogenic role in hypertension. ... Angiotensin II stimulates a hypertrophic response in cultured vascular smooth muscle cells. As part of the growth response, ...
Vascular smooth muscle cells contribute to the formation of atherosclerotic plaques by proliferating in response to vascular ... Introduction of vascular smooth muscle cells expressing recombinant genes in vivo.. G Plautz, E G Nabel, G J Nabel ... Vascular smooth muscle cells from the inbred Yucatan minipig were infected in vitro with an amphotropic, replication-defective ... Vascular smooth muscle cells expressing this recombinant gene were implanted, using a catheter, into denuded iliofemoral artery ...
... whereas they were highly mobile in proliferative vascular smooth muscle cells (as is typical for most cell types). Vascular ... TRPML1 channels initiate Ca2+ sparks in vascular smooth muscle cells. By Pratish Thakore, Harry A. T. Pritchard, Caoimhin S. ... TRPML1 channels initiate Ca2+ sparks in vascular smooth muscle cells. By Pratish Thakore, Harry A. T. Pritchard, Caoimhin S. ... TRPML1 channels initiate Ca2+ sparks in vascular smooth muscle cells Message Subject. (Your Name) has forwarded a page to you ...
... including smooth muscle cells. Tissue factor expression on the smooth muscle cell surface could be of pathological significance ... LDL Increases Inactive Tissue Factor on Vascular Smooth Muscle Cell Surfaces. Marc S. Penn, Chandrashekhar V. Patel, Mei-Zhen ... LDL Increases Inactive Tissue Factor on Vascular Smooth Muscle Cell Surfaces. Marc S. Penn, Chandrashekhar V. Patel, Mei-Zhen ... Active oxygen species stimulate vascular smooth muscle cell growth and proto-oncogene expression. Circ Res. 1992;70:593-599. ...
Drug delivery system N-acetylglucosamine Lectin Restenosis Vascular smooth muscle cells This is a preview of subscription ... Targeting N-acetylglucosamine-bearing polymer-coated liposomes to vascular smooth muscle cells. ... are specifically taken up by vascular smooth muscle cells (VSMCs). Flow cytometric analysis revealed that GlcNAc-Ls were taken ... Furthermore, GlcNAc-Ls were intravenously administered to mice that had undergone wire-mediated vascular injury. GlcNAc-Ls ...
Vascular smooth muscle is the type of smooth muscle that makes up most of the walls of blood vessels. Vascular smooth muscle ... are vascular smooth muscle cell derived. Mural cell Bennett, M. R; Sinha, S; Owens, G. K (2016). "Vascular smooth muscle cells ... Image of smooth muscle in the arterial walls Smooth muscle in stomach wall. ... Vascular smooth muscle contracts or relaxes to change both the volume of blood vessels and the local blood pressure, a ...
The recent development of coculture systems of endothelial cells and vascular smooth muscle cells can be extended to high- ... and biologic interactions between endothelial cells and vascular smooth muscle cells are discussed. Key considerations in the ... design of high-throughput systems are presented, and selected examples are discussed.Keywords: endothelium, vascular smooth ... throughput systems for the identification of compounds for angiogenesis, vascular repair, and hypertension. In this review, the ...
... in occluding vascular diseases. Here we identified a positive role of ALDH1A3... ... Vascular smooth muscle cell (VSMC) proliferation promotes intimal hyperplasia (IH) ... Vascular Smooth Muscle Cell Proliferation.". Vascular smooth muscle cell (VSMC) proliferation promotes intimal hyperplasia (IH ... A GATA transcription factor that is expressed predominately in SMOOTH MUSCLE CELLS and regulates vascular smooth muscle CELL ...
To investigate this hypothesis, we exposed primary cultures of vascular smooth muscle cells (VSMCs) from wistar kyoto (WKY) and ... studies support the hypothesis that Cd can be a risk factor of hypertension through dysfunction of vascular smooth muscle cells ... vascular smooth muscle cells Protein kinase C; mitogen-activated protein kinase; ERK 1; ERK 2; vascular smooth muscle cells ... Cadmium Toxicity on Arterioles Vascular Smooth Muscle Cells of Spontaneously Hypertensive Rats. Benny Washington 1,* , Shunta ...
  • The vascular smooth muscle cell (VSMC) is a highly specialized cell whose principal function is contraction. (genome.jp)
  • Impairment of vascular smooth muscle cells (VSMC) is recognized as a predisposition factor for atherosclerosis development. (scirp.org)
  • The modulation of adipokine secretions in the adipose tissue that is linked to metabolic alterations may alter the physiology of VSMC and thus accelerate the development of metabolic-related vascular diseases. (scirp.org)
  • Specifically, postmortem studies have identified profound loss of vascular smooth muscle cells (VSMC) in the medial layer of large arteries, such as the aorta and carotid arteries, with replacement by collagen and extracellular matrix. (pnas.org)
  • Vascular smooth muscle cell (VSMC) proliferation promotes intimal hyperplasia (IH) in occluding vascular diseases. (bioportfolio.com)
  • This study is to determine the roles and mechanisms of miR-135a-5p intervention in attenuating VSMC proliferation and vascular remodeling in spontaneously hypertensive rats (SHRs). (nature.com)
  • Silencing of miR-135a-5p attenuates VSMC proliferation and vascular remodeling in SHRs via disinhibition of FNDC5 transcription. (nature.com)
  • Methods and Results: Vascular smooth muscle cell (VSMC) proliferation and neointimal hyperplasia were evaluated in cultured VSMCs and wire-injured mouse carotid arteries from wild-type (WT, C57BL/ 6J), AMPK alpha 2(-/-), and AMPK alpha 1(-/-) mice. (rti.org)
  • The phenolic compound esculetin is known to inhibit the proliferation of vascular smooth muscle cells (VSMC). (sigmaaldrich.com)
  • Obesity is characterized by poor collateral vessel formation, a process involving vascular endothelial growth factor (VEGF) action on vascular smooth muscle cells (VSMC). (mdpi.com)
  • Free fatty acids are involved in the pathogenesis of obesity vascular complications, and we have aimed to clarify whether oleic acid (OA) enhances VEGF synthesis/secretion in VSMC, and whether this effect is impaired in obesity. (mdpi.com)
  • We previously reported that NOX activator 1 (NOXA1) is the critical functional homolog of p67phox for NADPH oxidase activation in mouse vascular smooth muscle cells (VSMC). (elsevier.com)
  • Objectives Excessive proliferation vascular smooth muscle cells (VSMC) can promote the development of atherosclerosis. (bmj.com)
  • Notch receptor-ligand interactions are a highly conserved mechanism, originally described in developmental studies using Drosophilae, that regulate inter-cell communication and dictate, in part, vascular smooth muscle cell (VSMC) fate in response to mechanical stimuli. (dcu.ie)
  • VSMC differentiation is a crucial developmental process regulating angiogenesis and vasculogenesis, with phenotypic modulation of SMC a key factor in vascular pathology. (dcu.ie)
  • The sympathetic nervous system has been shown to exert a trophic influence on vascular smooth muscle cells (VSMC). (lu.se)
  • Neuropeptid Y (NPY) verstärkt die Proliferation vaskulärer glattmuskulärer Zellen („vascular smooth muscle cells", VSMC) unmittelbar durch Bindung an Y1-Rezeptoren. (springer.com)
  • Vascular smooth muscle cells were transduced with miR‐145 inhibitor and mimic to determine the effect of miR‐145 expression on VSMC proliferation. (bionity.com)
  • Mechanistically, ALDH2 inhibition ablated pathological vascular smooth muscle cell (VSMC) phenotypical switch through interaction with myocardin, a determinant of VSMC contractile phenotype. (onmedica.com)
  • To elucidate the patho-physiological role of parathyroid-hormone-related peptide (PTHrP) in vascular system, it is essential to investigate on the molecular mechanism of PTHrP receptor mediated signal transductionin in vascular smooth muscle cells (VSMC) or endotherial cells. (nii.ac.jp)
  • We examined the electrophysiological and transcriptional mechanisms by which KCa3.1 regulates vascular smooth muscle cell (VSMC) proliferation. (pubmedcentralcanada.ca)
  • Vascular smooth muscle cell (VSMC) proliferation is a crucial event in the development of vascular diseases such as atherosclerosis and restenosis ( 11 , 12 ). (pubmedcentralcanada.ca)
  • 1 This VSMC behavior is a key mechanism for the establishment of vascular tone and the autoregulation of blood flow ( 8 ). (physiology.org)
  • It is generally assumed that, in the myogenic response, a perturbation in intravascular pressure changes vascular wall tension/stress, which then triggers the contraction of the VSMC. (physiology.org)
  • Medial vascular calcification, associated with enhanced mortality in chronic kidney disease (CKD), is fostered by osteo-/chondrogenic transdifferentiation of vascular smooth muscle cells (VSMCs). (jci.org)
  • Aortic vascular smooth muscle cells (vascular smooth muscle cells [VSMCs]) were isolated from Sprague-Dawley rats as described previously. (ahajournals.org)
  • We used passages 3 to 8 after phenotyping by staining VSMCs for muscle-specific α-actin (Dako) and desmin (Boehringer-Mannheim). (ahajournals.org)
  • To develop a drug delivery system targeted to injured blood vessels, we examined whether N -acetylglucosamine (GlcNAc)-bearing polymer-coated liposomes (GlcNAc-Ls) are specifically taken up by vascular smooth muscle cells (VSMCs). (springer.com)
  • To investigate this hypothesis, we exposed primary cultures of vascular smooth muscle cells (VSMCs) from wistar kyoto (WKY) and spontaneously hypertensive rats (SHR) to increased concentrations of CdCl 2 on cell viability, expression of mitogen-activated protein kinases (MAPKs/ERK 1 & 2), and protein kinase C (PKC) which are activated by Cd in several cell types. (mdpi.com)
  • Proliferation of vascular smooth muscle cells (VSMCs) greatly contributes to vascular remodeling in hypertension. (nature.com)
  • HG-induced NF-kappaB activation was inhibited by a protein kinase C inhibitor, calphostin C. These results suggest that hyperglycemia-induced activation of NF-kappaB in VSMCs may be a key mechanism for the accelerated vascular disease observed in diabetes. (diabetesjournals.org)
  • Objective- Hyperphosphatemia and inorganic phosphate (Pi) transport by vascular smooth muscle cells (VSMCs) have been implicated in the pathogenesis of vascular calcification. (ahajournals.org)
  • Because dys-regulation of RhoA/Rho kinase pathway is implicated in increased vascular contractility, we examined whether TCTP induces alterations in RhoA pathway in vascular smooth muscle cells (VSMCs). (mdpi.com)
  • Nevertheless, MSCs have the potential to differentiate into VSMCs and may be the source of proliferating VSMCs during neointima formation after vascular injury. (medicalxpress.com)
  • The present study was carried out to examine whether As-IV can reverse Ang II-induced mitochondrial dysfunction in vascular smooth muscle cells (VSMCs) and to elucidate the underlying molecular mechanisms. (spandidos-publications.com)
  • The mitochondria are also regarded as critical regulators of cell death and are the major cellular source of reactive oxygen species (ROS) ( 1 ), which cause damage to mitochondrial DNA (mtDNA) in human vascular smooth muscle cells (VSMCs) in a number of cardiovascular pathologies ( 2 ). (spandidos-publications.com)
  • The type III sodium-dependent phosphate transporter, PiT-1, is required for elevated Pi-induced osteochondrogenic differentiation and matrix mineralization in vascular smooth muscle cells (VSMCs). (washington.edu)
  • In this thesis we studied how different substances of special interest in the pathogenesis of vascular disease interact and regulate each other's expressions in endothelial cells and vascular smooth muscle cells (VSMCs). (diva-portal.org)
  • Neuropeptide Y (NPY) intensifies the proliferation of vascular smooth muscle cells (VSMCs) directly by binding with Y1 receptors. (springer.com)
  • Proliferation and migration of vascular smooth muscle cells (VSMCs) play crucial roles in the development of vascular restenosis. (selleckchem.com)
  • Collectively, we demonstrated that Akt signaling pathway mediates WISP1-induced migration and proliferation of human VSMCs, suggesting that WISP1 may act as a novel potential therapeutic target for vascular restenosis. (selleckchem.com)
  • Vascular smooth muscle cells (VSMCs) play an important role in the good performance of the vasculature. (eurekamag.com)
  • Given the close association of small CaP particles with vascular smooth muscle cells (VSMCs) in atherosclerotic fibrous caps, we aimed to determine if CaP particles affected pro-inflammatory signalling in human VSMCs. (open.ac.uk)
  • TNF‑α is pleiotropic and mediates inflammation and proliferation in various cell types, such as vascular smooth muscle cells (VSMCs). (spandidos-publications.com)
  • The vasculature is predominantly comprised of vascular smooth muscle cells (VSMCs), and these cells are involved in the maintenance of vessel tone and blood pressure ( 1 , 2 ). (spandidos-publications.com)
  • Switching of vascular smooth muscle cells (VSMCs) from a contractile phenotype to an adverse proliferative phenotype is a hallmark of atherosclerosis or vascular restenosis. (bionity.com)
  • Atherosclerotic samples and VSMCs had decreased expression of contractile markers calponin and alpha smooth muscle actin (α‐SMA) and MYOCD. (bionity.com)
  • Our previous studies have demonstrated that the GPI (glycosylphosphatidylinositol)-linked uPAR [uPA (urokinase-type plasminogen activator) receptor], which can be found in lipid rafts and in non-raft fractions, can mediate the differentiation of VSMCs (vascular smooth muscle cells) towards a pathophysiological de-differentiated phenotype. (biochemj.org)
  • Integrin-mediated mechanotransduction in vascular smooth muscle cells (VSMCs) plays an important role in the physiological control of tissue blood flow and vascular resistance. (physiology.org)
  • mechanotransduction in vascular smooth muscle cells (VSMCs) is a fundamental mechanism underlying the vascular myogenic response ( 9 ), in which vascular smooth muscle contracts in response to increased intralumenal pressure or relaxes in response to decreased pressure ( 11 , 21 ). (physiology.org)
  • Inducible interleukin-1 gene expression in human vascular smooth muscle cells. (harvard.edu)
  • Transdifferentiated Human Vascular Smooth Muscle Cells are a New Potential Cell Source for Endothelial Regeneration. (sigmaaldrich.com)
  • The expression of smouth muscle cell specific a-atin, calponin, myosin and smoothdin was examined by immunocytochemistry, Western blot analysis and quantitative real time PCR in human vascular SMC cultured under static conditions following over-expression of constitutively active Notch 1 and 3 receptors. (dcu.ie)
  • Insulin-like growth factor binding proteins-2 to -6 are expressed by human vascular smooth muscle cells. (diva-portal.org)
  • We have investigated the expression and secretion of insulin-like growth factor binding proteins (IGFBPs-1 to -6) in human vascular smooth muscle cells (hVSMCs) cultured from human renal arteries. (diva-portal.org)
  • Vascular-specific smoothelin-B is the first smooth muscle cell marker that disappears when vascular tissues are compromised, for example, in atherosclerosis or restenosis. (biomedsearch.com)
  • A polyphenol in oat may prevent atherosclerosis by inhibiting smooth muscle cell proliferation and enhancing nitric oxide production. (greenmedinfo.com)
  • Excessive proliferation of vascular smooth muscle cells contributes to the progression of pathological conditions, such as vascular inflammation, plaque formation, atherosclerosis, restenosis, and pulmonary hypertension. (wikipedia.org)
  • Therapeutic strategies targeting cell cycle progression and mitogenic stimuli have been developed and evaluated in animal models of atherosclerosis and vascular injury, and several clinical studies. (thefreelibrary.com)
  • This suggests that expression of class II antigen is part of a phenotypic change in smooth muscle cells in atherosclerosis. (unboundmedicine.com)
  • TY - JOUR T1 - Expression of class II transplantation antigen on vascular smooth muscle cells in human atherosclerosis. (unboundmedicine.com)
  • There is growing evidence that aging promotes vascular inflammation ( 9 , 10 , 12 , 14 - 16 , 43 ) and development of atherosclerosis and that mitochondrial oxidative stress may contribute to proinflammatory phenotypic alterations in aged vessels. (physiology.org)
  • Dzau VJ, Braun-Dullaeus RC, Sedding DG (2002) Vascular proliferation and atherosclerosis: new perspectives and therapeutic strategies. (springer.com)
  • Our data suggest that homocysteine induces smooth muscle cell growth through a pathway that is independent of H_2O_2, that involves MAPK kinase activation, and that results in accelerated atherosclerosis. (iospress.com)
  • TNF-α is a pleiotropic inflammatory cytokine that has been reported to serve a pathophysiological role in vascular atherosclerosis ( 9 , 10 ). (spandidos-publications.com)
  • Under NE binding α 1 receptors cause vasoconstriction i.e. contraction of the vascular smooth muscle cells decreasing the diameter of the vessels. (wikidoc.org)
  • Although elastase-induced degradation of extracellular matrix proteins and the ensuing inflammation of the aortic wall have been implicated as possible causes of the aortic dilation in AAA, little is known regarding the effects of elastase on the mechanisms of aortic smooth muscle contraction. (ovid.com)
  • The purpose of this study was to test the hypothesis that elastase promotes aortic dilation by inhibiting the Ca 2+ mobilization mechanisms of smooth muscle contraction. (ovid.com)
  • These data suggest that elastase promotes aortic relaxation by inhibiting the Ca 2+ entry mechanism of vascular smooth muscle contraction, and thus further explain the role of increased elastase activity during the early development of AAA. (ovid.com)
  • Angiotensin II (Ang II) has been shown to participate in physiological processes, such as sodium and water homeostasis, and vascular contraction, as well as in pathophysiological processes, including hypertrophic cell growth, endothelial dysfunction, and cardiovascular and renal remodeling ( 3 ). (spandidos-publications.com)
  • how is vascular smooth muscle contraction triggered? (brainscape.com)
  • Angiotensin II stimulates a hypertrophic response in cultured vascular smooth muscle cells. (ahajournals.org)
  • Kinetic analysis of internalization, recycling and redistribution of atrial natriuretic factor-receptor complex in cultured vascular smooth-muscle cells. (portlandpress.com)
  • Abstract In this review, the role of tyrosine kinases in angiotensin II-mediated signal transduction pathways in vascular smooth muscle is discussed. (ahajournals.org)
  • It was presented in abstract form at Experimental Biology 99, Washington, DC, April 1999 [Grant SL, Griendling KK, Lassègue B, Ushio-Fukai M and Alexander RW (1999) Angiotensin II regulates RGS expression in vascular smooth muscle cells]. (aspetjournals.org)
  • Vascular smooth muscle cells (SMCs) exhibit extensive phenotypic diversity and rapid growth during embryonic development, but maintain a quiescent, differentiated state in adult. (thefreelibrary.com)
  • Vascular smooth muscle cell (SMC) composes the majority of the vascular wall and retains phenotypic plasticity in response to various stimuli. (sigmaaldrich.com)
  • The Notch signaling pathway may therefore represent a novel mechanism for targeting vascular disorders in which SMC phenotypic diversity occurs in vivo. (dcu.ie)
  • Little is known about the phenotypic changes that occur in vascular smooth muscle cells (SMCs) as the developing aorta undergoes the transition from a loosely organized, highly replicative tissue to a morphologically mature, quiescent tissue. (ahajournals.org)
  • Epigenetic control of smooth muscle cell differentiation and phenotypic switching in vascular development and disease. (semanticscholar.org)
  • An association has been curated linking Dnmt1 and negative regulation of vascular associated smooth muscle cell differentiation involved in phenotypic switching in Rattus norvegicus. (mcw.edu)
  • Abnormal vascular smooth muscle cell (SMC) proliferation and migration contribute to the development of restenosis after percutaneous transluminal coronary angioplasty and accelerated arteriopathy after cardiac transplantation. (jci.org)
  • Nitric oxide (NO) is of crucial importance for smooth muscle cell (SMC) function and exerts numerous, and sometimes opposing, effects on vascular restenosis. (nih.gov)
  • Although cGMP-dependent protein kinase type I (cGKI) is a principal effector of NO, the molecular pathway of vascular NO signaling in restenosis is unclear. (nih.gov)
  • The purpose of this study was to examine the functional role of the smooth muscle cGMP/cGKI signaling cascade in restenosis of vessels. (nih.gov)
  • The genetic and pharmacological manipulation of the cGMP/cGKI signaling indicates that this pathway is not involved in the protective effects of NO, suggesting that NO affects vascular remodeling during restenosis via alternative mechanisms. (nih.gov)
  • Interest in the role that tissue factor expressed by smooth muscle cells (SMC) may play in atherosclerotic lesion growth, restenosis after angioplasty, and acute coronary syndrome has been heightened by multiple observations. (ahajournals.org)
  • The pathogenesis of vascular proliferative diseases involves the proliferation and migration of medial vascular SMCs into the vessel intima, possibly reinstating their embryonic gene expression programs. (thefreelibrary.com)
  • To evaluate which signalling molecules are involved in homocysteine induced atherosclerotic changes during the pathogenesis of vascular diseases, we examined homocysteine induced smooth muscle cell proliferation in the presence of different signal transduction inhibitors. (iospress.com)
  • Evidence suggests that the concentration of extracellular Ca 2+ and vascular smooth muscle cells play a pivotal role in the pathogenesis of vascular calcification. (endocrine-abstracts.org)
  • Inhibition of Ca2+ uptake into A7r5 vascular smooth muscle cells by farnesol: Lack of effect on membrane fluidity and Ca2+-ATPase activities," Journal of Hypertension , vol. 15, no. 12, pp. 1723-1728, 1997. (hindawi.com)
  • We tested the hypothesis that IL-10 may also inhibit vascular smooth muscle cell (SMC) activation via the inhibition of the NF-kappaB/I-kappaB system. (mendeley.com)
  • Inhibition of SGK1 may, thus, reduce the burden of vascular calcification in CKD. (jci.org)
  • One of these non-genomic effects is the inhibition of adrenergic agonist transport into airway vascular smooth muscle cells with an increase of adrenergic agonist concentrations at adrenergic receptor sites and enhance the physiological effects of endogenous adrenergic agonists (e.g. locally released norepinephrine from noradrenergic neurons) or exogenous adrenergic agonists (e.g. inhaled beta-adrenergic agonists). (clinicaltrials.gov)
  • Either inhibition of miR-135a-5p or upregulation of FNDC5 may be a therapeutically strategy in attenuating vascular remodeling and hypertension. (nature.com)
  • p38 MAPK activation is required for esculetin-induced inhibition of vascular smooth muscle cells proliferation. (sigmaaldrich.com)
  • These findings suggest that Notch receptors modulate vascular SMC phenotype in vitro and cyclic strain enhances SMC differentiation in part through inhibition of Notch receptor expression. (dcu.ie)
  • In this study, we tested the hypothesis that inhibition of glucose-6-phosphate dehydrogenase (G6PD), a major source of NADPH in the cell, prevents 20-HETE synthesis and 20-HETE-induced proinflammatory signaling that promotes secretory phenotype of vascular smooth muscle cells. (physiology.org)
  • In summary, our findings indicate that 20-HETE elicited mitochondrial superoxide production and promoted secretory phenotype of vascular smooth muscle cells by activating MAPK1-Elk-1, all of which are blocked by inhibition of G6PD. (physiology.org)
  • Nitric oxide did not regulate the expression of IGFBPs and IGF-I-induced smooth muscle cell proliferation was not affected by inhibition of endogenous NO production. (diva-portal.org)
  • This pathway mediated the Pak-dependent inhibition of phosphodiesterase type 5, a process that favored RhoA inactivation and the subsequent depolymerization of the F-actin cytoskeleton in vascular smooth muscle cells. (csic.es)
  • Curcumin inhibits ox-LDL stimulated vascular smooth muscle cell proliferation associated with arteriosclerosis. (greenmedinfo.com)
  • Honokiol inhibits vascular smooth muscle cell proliferation, indicating it may have a role in arteriosclerosis treatment. (greenmedinfo.com)
  • Thank you for your interest in spreading the word on Arteriosclerosis, Thrombosis, and Vascular Biology. (ahajournals.org)
  • Your Name) thought you would like to see the Arteriosclerosis, Thrombosis, and Vascular Biology web site. (ahajournals.org)
  • Arteriosclerosis, Thrombosis, and Vascular Biology 9 (3) (May 1): 279-288. (harvard.edu)
  • Vascular smooth muscle cells (SMCs) and pericytes are essential for the stabilisation of nascent immature endothelial tubes. (nih.gov)
  • Despite the intense interest in the utility of human embryonic stem cells (ESCs) for vascular regenerative medicine, ESC-derived vascular SMCs have received much less attention than ECs. (nih.gov)
  • The junctophilins are critically important for cardiac and skeletal muscle function, but little is known about how these proteins influence vascular smooth muscle cells (SMCs). (pnas.org)
  • Here, we report that JPH2 is the most abundant junctophilin isotype in native smooth muscle cells (SMCs) isolated from cerebral arteries and that acute knockdown diminishes the area of sites of interaction between the SR and plasma membrane. (pnas.org)
  • We investigated whether the absence of cGKI in SMCs would affect vascular remodeling after carotid ligation or removal of the endothelium. (nih.gov)
  • Here, we investigated the function of TRPML1 channels in fully differentiated contractile vascular smooth muscle cells (SMCs). (sciencemag.org)
  • Human SMCs are first dedifferentiated for 4 days to achieve a vascular progenitor state expressing CD34, by introducing transcription factors OCT4, SOX2, KLF4 and c-MYC. (sigmaaldrich.com)
  • Further comprehensive analysis indicates that mesenchymal-to-epithelial transition is requisite to initiate SMCs reprogramming into vascular progenitors and that members of the Notch signalling pathway regulate further differentiation of the progenitors into endothelial lineage. (sigmaaldrich.com)
  • Together, we provide the first evidence of the feasibility of the conversion of human SMCs towards endothelial lineage through an intermediate vascular progenitor state induced by reprogramming. (sigmaaldrich.com)
  • Previous studies using rigorous smooth muscle cell (SMC) lineage tracing have shown abundant SMC investment into atherosclerotic lesions, where SMCs contribute to the formation of a protective fibrous cap. (jci.org)
  • Vascular smooth muscle cells (SMCs) populate in the media of the blood vessel, and play an important role in the control of vasoactivity and the remodeling of the vessel wall. (techscience.com)
  • Bone marrow mesenchymal stem cell (MSC) is a potential cell source for vascular regeneration therapy, and may be used to generate SMCs to construct tissue-engineered vascular grafts for blood vessel replacements. (techscience.com)
  • In the present study, we have characterized the in vivo pattern of SMC replication during intrauterine and neonatal aortic development in the rat and have cultured and assessed the in vitro growth properties of embryonic, fetal, and neonatal vascular SMCs. (ahajournals.org)
  • Taken together, the data describe a unique embryonic growth phenotype of vascular SMCs and suggest that the replication of aortic SMCs during intrauterine development is self driven, self regulated, and controlled by a developmental timing mechanism. (ahajournals.org)
  • The conversion of SMCs from the embryonic to the late fetal/adult growth phenotype will likely be found to be an important component of a developmental system controlling vascular morphogenesis. (ahajournals.org)
  • They are increasingly used to monitor the smooth muscle cell differentiation process to a contractile or synthetic phenotype. (biomedsearch.com)
  • A GATA transcription factor that is expressed predominately in SMOOTH MUSCLE CELLS and regulates vascular smooth muscle CELL DIFFERENTIATION. (bioportfolio.com)
  • These findings suggest that loss-of-function mutations or decreased expression of JPH2 could contribute to vascular pathologies such as systemic hypertension and vascular cognitive impairment. (pnas.org)
  • Vascular smooth muscle cell hypertrophy is a normal compensatory state that may play a pathogenic role in hypertension. (ahajournals.org)
  • The recent development of coculture systems of endothelial cells and vascular smooth muscle cells can be extended to high-throughput systems for the identification of compounds for angiogenesis, vascular repair, and hypertension. (dovepress.com)
  • Conditional deletion of smooth muscle Cullin-3 causes severe progressive hypertension. (bioportfolio.com)
  • Patients with mutations in Cullin-3 (CUL3) exhibit severe early onset hypertension but the contribution of the smooth muscle remains unclear. (bioportfolio.com)
  • The present studies support the hypothesis that Cd can be a risk factor of hypertension through dysfunction of vascular smooth muscle cells under certain conditions. (mdpi.com)
  • MiR-135a-5p knockdown in SHRs attenuated hypertension, normalized FNDC5 expressions and inhibited vascular smooth muscle proliferation, and alleviated vascular remodeling. (nature.com)
  • Vascular remodeling in hypertension: mechanisms and treatment. (nature.com)
  • Vascular smooth muscle remodeling in conductive and resistance arteries in hypertension. (nature.com)
  • Vascular Smooth Muscle Function in Hypertension Edition by Theodora Szasz and Publisher Morgan & Claypool Life Sciences. (vitalsource.com)
  • Modulation of TCTP may offer a therapeutic target for hypertension and in vascular contractility dysfunction. (mdpi.com)
  • The results suggest that abnormal biochemistry of the plasma membrane isolated from small arteries of hypertensive animals, which appears to involve a defect of calcium regulation across the vascular plasma membrane, is probably associated with the pathogenesis of hypertension. (aspetjournals.org)
  • HDAC4 mediates development of hypertension via vascular inflammation in spontaneous hypertensive rats. (semanticscholar.org)
  • Compared to wild-type mice, NOD2-deficient mice developed severe pulmonary hypertension with exaggerated elevation of right ventricular systolic pressure, profound right ventricular hypertrophy and striking vascular remodeling after exposure to hypoxia. (oncotarget.com)
  • Our findings revealed that the absence of NOD2 exacerbated hypoxia-induced PASMC proliferation, pulmonary hypertension and vascular remodeling, but had no effect on PASMC migration or contractility. (oncotarget.com)
  • This text also explains how smooth muscle cells regulate their contractile activity through regulation of calcium ion fluxes and the interaction, at the molecular level, of calcium ions with regulatory proteins associated with the contractile apparatus. (elsevier.com)
  • K. D. Wu, D. Bungard, and J. Lytton, "Regulation of SERCA Ca2+ pump expression by cytoplasmic Ca2+ in vascular smooth muscle cells," The American Journal of Physiology - Cell Physiology , vol. 280, no. 4, pp. (hindawi.com)
  • Both proteins interacted with rabbit skeletal troponin C in the presence and absence of Ca2+, but they did not interact with troponin I. These results suggest that the novel protein, which is designated calponin, may be a specialized component of smooth muscle thin filament involved in the regulation of contractile apparatus. (nih.gov)
  • Na+, K(+)-adenosine triphosphatase regulation in hypertrophied vascular smooth muscle cells. (ahajournals.org)
  • Ca 2+ sparks in vascular smooth muscle cells are critical for blood vessel dilation and for blood pressure regulation. (sciencemag.org)
  • Regulation of smooth muscle cells in development and vascular disease: current therapeutic strategies. (thefreelibrary.com)
  • Because of morphologic evidence for immune-activated (class II+) SMC in vascular lesions, we studied the regulation by cytokines of MHC gene expression in SMC cultured from human vessels. (harvard.edu)
  • Aorta of TCTP-TG exhibited hypercontractile response compared to that of non-transgenic mice (NTG) suggesting dys-regulation of signaling pathways involved in the vascular contractility by TCTP. (mdpi.com)
  • Maeng J, Sheverdin V, Shin H, Ha I, Bae SS, Yang-Yen H-F, Lee K. Up-Regulation of Rhoa/Rho Kinase Pathway by Translationally Controlled Tumor Protein in Vascular Smooth Muscle Cells. (mdpi.com)
  • The focus of this project is to determine the role of Ca2+ in the regulation of SMA in resident non-muscle cell types of the heart. (osu.edu)
  • In addition, regulation of at least one of these transcription factors, YB-1, in non-muscle cells may be controlled by its relative concentration within the nucleus and cytoplasm. (osu.edu)
  • Understanding the hemodynamic regulation of SMC and MSC functions will provide a basis for the development of new vascular therapies and for the construction of tissue-engineered vascular grafts. (techscience.com)
  • These findings identify a p22 phox -containing NADH oxidase as a source for cytokine-induced free radical production in vascular smooth-muscle cells and clarify some of the mechanisms involved in the regulation of vascular oxidase activity. (biochemj.org)
  • Thus, RGS2 is a likely candidate for negative regulation of the G proteins coupled to the Ang II type 1 receptor in vascular smooth muscle cells. (aspetjournals.org)
  • Regulation of this protein may be of critical importance in modulating the role of Ang II in vascular disease. (aspetjournals.org)
  • This review begins with developmental insights into a range of smooth muscle progenitors from studies on embryos and ESC differentiation systems. (nih.gov)
  • By using CRISPR-Cas9 genome editing and in vitro smooth muscle differentiation assay, we demonstrate that CD146 regulates the balance between proliferation and differentiation. (ovid.com)
  • Ductus Arteriosus: Advanced differentiation of smooth muscle cells demonstrated by myosin heavy chain isoform expression in rabbits. (nii.ac.jp)
  • We investigated the role of Notch 1 and 3 receptor signaling in controlling vascular SMC differentiation in vitro, and established a role for cyclic strain induced changes in Notch in mediating this response. (dcu.ie)
  • DNA Methyltransferase 1 Is Essential For Differentiation Of Gastrointestinal Smooth Muscle, But Not Required For Maintaining The Differentiated State In Mus Musculus. (semanticscholar.org)
  • We conclude that corticosterone induces rapid mineralocorticoid receptor signaling in vascular smooth muscle cells that involves mitogen-activated protein kinase kinase/extracellular signal-regulated kinase-dependent pathways. (ahajournals.org)
  • Klotho deficiency induces arteriolar hyalinosis in a trade-off with vascular calcification. (bioportfolio.com)
  • BACKGROUND AND OBJECTIVES: This study was performed to investigate the antiproliferative effect of lovastatin on vascular smooth muscle cell, especially to determine whether lovastatin induces apoptosis in vascular smooth muscle cell and the products of mevalonate pathway can reverse the antiproliferative effect of lovastatin. (koreamed.org)
  • Objective: This study tested the hypothesis that hypoxia induces redox changes that differ among subcellular compartments in pulmonary (PASMCs) and systemic (SASMCs) smooth muscle cells. (luriechildrens.org)
  • Similarly, Sgk1 deficiency blunted vascular calcification in apolipoprotein E-deficient mice after subtotal nephrectomy. (jci.org)
  • These observations identified SGK1 as a key regulator of vascular calcification. (jci.org)
  • SGK1 promoted vascular calcification, at least partly, via NF-κB activation. (jci.org)
  • Evaluation of the calcifying effect of phosphorus on vascular smooth muscle and detect the association between serum phosphorus and valvular and vascular calcification in end stage renal d. (bioportfolio.com)
  • Vascular calcification (VC), the accumulation of calcium phosphate products in the wall of arteries, is a common complication of diabetes and chronic kidney disease that contributes to their morbidity and mortality. (ahajournals.org)
  • Vascular calcification (VC) is prevalent in chronic kidney disease and elevated serum inorganic phosphate (Pi) is a recognized risk factor. (washington.edu)
  • The research presented in this thesis addresses the role of PiT-1 in vascular calcification mechanisms. (washington.edu)
  • Both proteins shared a common antigenic determinant with COOH-terminal segments of rabbit skeletal and bovine cardiac troponin T and bound to the immobilized smooth muscle tropomyosin. (nih.gov)
  • ALDH1A3 Regulations of Matricellular Proteins Promote Vascular Smooth Muscle Cell Proliferation. (bioportfolio.com)
  • Thus interaction between integrins and specific matrix proteins is responsible for sensing mechanical strain in vascular smooth muscle cells. (jci.org)
  • The reversible inhibitory effects of elastase, particularly in the presence of saturating concentrations of elastin, suggest that they are not due to dissolution of the extracellular matrix or permanent damage to the smooth muscle contractile proteins. (ovid.com)
  • One of these proteins, vascular smooth muscle alpha actin (SMA), is the predominant actin in smooth muscle, but is not normally expressed in the adult heart. (osu.edu)
  • Vascular endothelial growth factor (VEGF) and transforming growth factor-ß1 (TGF-ß1) regulated the expression of insulin-like growth factor-binding proteins (IGFBPs) in large vessel endothelial cells in a way that might cause an increased bioavailability of IGF-I locally in the subendothelial space. (diva-portal.org)
  • Vascular smooth muscle cell cultures were generated, and expression of microRNA‐145 (miR‐145), its target gene Kruppel‐Like Factor 5 (KLF5) and Myocardin (MYOCD, a smooth muscle‐specific transcriptional coactivator) were analysed using RT‐qPCR, along with expression of relevant proteins. (bionity.com)
  • Objective: The aim of this study was to determine the roles of AMPK alpha in the development of vascular neointima hyperplasia and to elucidate the underlying mechanisms. (rti.org)
  • Endothelial dysfunction is widely implicated in cardiovascular pathological changes and development of vascular disease. (sigmaaldrich.com)
  • L-type calcium channel expression depends on the differentiated state of vascular smooth muscle cells," The FASEB Journal , vol. 12, no. 7, pp. 593-601, 1998. (hindawi.com)
  • Evidence was not found for a direct relationship between the potentiating action of HC and membrane depolarization or the availability of extracellular calcium for the muscle response produced by a stimulating agent. (aspetjournals.org)
  • Deoxycorticosterone treatment alone slightly enhanced alkaline phosphatase activity but did not alter calcium accumulation, weight or protein content of plasma membranes from arterial smooth muscle. (aspetjournals.org)
  • The intermediate conductance calcium-activated potassium channel KCa3.1 contributes to a variety of cell activation processes in pathologies such as inflammation, carcinogenesis, and vascular remodeling. (pubmedcentralcanada.ca)
  • Significantly, restriction of mitochondrial motility using the fission inhibitor Mdivi-1, inhibited vascular smooth muscle proliferation in both single cells and in the intact resistance artery. (strath.ac.uk)
  • Lysosomes in contractile vascular smooth muscle cells were immobile and localized in close proximity to an ion channel that is part of the Ca 2+ spark-generating pathway, whereas they were highly mobile in proliferative vascular smooth muscle cells (as is typical for most cell types). (sciencemag.org)
  • Conclusions −These results suggest a novel 2-step pathway for increased tissue factor activity on smooth muscle cell surfaces in which lipoproteins regulate synthesis of a latent tissue factor and oxidants activate the protein complex. (ahajournals.org)
  • METHODS AND MATERIALS: Lovastatin only and lovastatin with one of the products of mevalonate pathway such as isopentenyl adenine, farnesol, mevalonate, cholesterol were added respectively in cultured rat vascular smooth muscle cells stimulated with 10% fetal calf serum. (koreamed.org)
  • We show that MAPK kinase pathway is involved in homocysteine induced DNA synthesis and proliferation of vascular smooth muscle cells in the presence of the peroxide scavenging enzyme, catalase. (iospress.com)
  • KCa3.1 is highly expressed in a variety of nonexcitable and proliferating cells ( 2 ), and an increase in KCa3.1 expression has been associated with cancer development, immune disorders, and vascular inflammation. (pubmedcentralcanada.ca)
  • This method, which provides for the introduction of genetically modified smooth muscle cells, can be used to define the biological effects of recombinant genes in the vessel wall and potentially to provide alternative treatments of vascular diseases. (ahajournals.org)
  • Because altered function of smooth muscle cells (SMC) accompanies certain vascular diseases, we tested whether SMC themselves might produce this hormone. (harvard.edu)
  • Vascular smooth muscle turnover has important implications for blood vessel repair and for the development of cardiovascular diseases, yet lack of specific transgenic animal models has prevented it's in vivo analysis. (ovid.com)
  • Vascular smooth muscle is innervated primarily by the sympathetic nervous system through adrenergic receptors ( adrenoceptors ). (wikidoc.org)
  • Antagonists of α 1 receptors ( doxazosin , prazosin ) cause vasodilation i.e. decrease in vascular smooth muscle tone with increase of vessel dimater and decrease of the blood pressure. (wikidoc.org)
  • Agonists of α 2 receptors in the vascular smooth muscle lead to vasoconstriction. (wikidoc.org)
  • This presynaptic effect is predominant and completely overrides the vasoconstrictive effect of the α 2 receptors in the vascular smooth muscle. (wikidoc.org)
  • Agonism at β 2 receptors causes vasodilation and hypotension , i.e. the effect is opposite of the one resulting from activation of α 1 and α 2 receptors in the vascular smooth muscle cells. (wikidoc.org)
  • Endothelin-1 (ET-1) is a powerful vasoconstricting peptide produced predominantly by vascular endothelial cells, that exerts its effect through the interaction with specific receptors, ETA. (bioportfolio.com)
  • Other receptors in this family include the α- and β-adrenergic receptors, the muscarinic acetylcholine receptor, the various serotonin receptors, and important vascular receptors such as the thrombin, bradykinin, and endothelin receptors. (ahajournals.org)
  • Rapamycin inhibits vascular smooth muscle cell migration. (jci.org)
  • IL-10 inhibits vascular smooth muscle cel. (mendeley.com)
  • IL-10 inhibits vascular smooth muscle cell activation in vitro and in vivo. (mendeley.com)
  • AlF4- inhibits influx of Ca2+ into vascular smooth muscle cells. (ucl.ac.uk)
  • In contrast, microanastomosis leads to early smooth muscle death and subsequent colonization of the vascular wall by proliferative adventitial cells that contribute to the repair. (ovid.com)
  • High speed fluorescence imaging of mitochondria in live vascular smooth muscle cells shows that the organelle undergoes significant re-organisation as cells become proliferative. (strath.ac.uk)
  • Bacterial lipopolysaccharide (LPS) has been shown to stimulate resting vascular smooth muscle cells (SMC) with the production of inflammatory cytokines and modulation of quiescent cells to the proliferative and synthetic phenotype. (thescipub.com)
  • Electronmicroscopy and confocal microscopy (en face Mitotracker staining) revealed that in aortas of F344 rats, a decline in mitochondrial biogenesis occurs with aging. (physiology.org)
  • 1. Isolated hind limbs of rats were perfused and vascular smooth muscle sensitivity to noradrenaline, methoxamine and potassium chloride was measured and dose-response curves were obtained. (clinsci.org)
  • Vascular Smooth Muscle: Metabolic, Ionic, and Contractile Mechanisms addresses the vascular smooth muscle function by describing plasma lipoprotein structure, synthesis, and transport in relation to the concepts of altered vascular smooth muscle lipid metabolism leading to the genesis of atherosclerotic disease. (elsevier.com)
  • The objective of this study was to characterize the dynamics and mechanisms of vascular smooth muscle turnover from the earliest stages of embryonic development to arterial repair in the adult. (ovid.com)
  • Whether AMPK alpha alters vascular neointima formation induced by vascular injury is unknown. (rti.org)
  • In limited wire-induced injury response, existing smooth muscle cells are the primary contributors to neointima formation. (ovid.com)
  • Vascular smooth muscle cell proliferation as a therapeutic target. (wikipedia.org)
  • This mitochondrial plasticity is an essential mechanism for the development of smooth muscle proliferation and therefore presents a novel therapeutic target against vascular disease. (strath.ac.uk)
  • We speculate that Trx1 may represent a novel therapeutic target for the vascular remodeling that underlies PH. (wku.edu)
  • 2004) Atherosclerotic plaque smooth muscle cells have a distinct phenotype. (scirp.org)
  • Vascular smooth muscle cells contribute to the formation of atherosclerotic plaques by proliferating in response to vascular injury and releasing growth-promoting factors. (ahajournals.org)
  • Background −Tissue factor, which is required for the initiation of the extrinsic coagulation cascade, is known to be upregulated in cells within atherosclerotic lesions, including smooth muscle cells. (ahajournals.org)
  • Recent studies have shown that the majority of cells within atherosclerotic plaque, the predominant cause of heart attack and stroke, are vascular smooth muscle cell derived. (wikipedia.org)
  • A large proportion of the cells of the human atherosclerotic plaque is assumed to be derived from medial smooth muscle cells. (unboundmedicine.com)
  • This indicates that smooth muscle cells of atherosclerotic plaques express DR antigen. (unboundmedicine.com)
  • SMC-specific deletion of Noxa1 in Apoe-/- mice (Noxa1SMC-/-/Apoe-/-) similarly decreased vascular ROS levels and atherosclerotic lesion size. (elsevier.com)
  • The next two chapters offer the reader a view of smooth muscle membrane properties in terms of the distribution, transport, and metabolic control of electrolytes and specific aspects of ion conductance and electrical activity. (elsevier.com)
  • with the technical assistance of LINZNER, U.: Oscillating fluxes and membrane potentials in vascular smooth muscle and cardiac muscle. (springer.com)
  • Additionally, we report here for the first time that 20-HETE repressed miR-143, which suppresses Elk-1 expression, and miR-133a, which is known to suppress synthetic/secretory phenotype of vascular smooth muscle cells. (physiology.org)
  • Nanomolar potency and selectivity of a Ca2+ release-activated Ca2+ channel inhibitor against store-operated Ca2+ entry and migration of vascular smooth muscle cells," British Journal of Pharmacology , vol. 164, no. 2, pp. 382-393, 2011. (hindawi.com)
  • MicroRNA26 attenuates vascular smooth muscle maturation via endothelial BMP signalling. (bioportfolio.com)
  • Angiotensin II, the dominant effector of the renin-angiotensin system, regulates numerous physiological responses, including salt and water balance, blood pressure, and vascular tone. (ahajournals.org)
  • Endothelial and smooth muscle cell ion channels in pulmonary vasoconstriction and vascular remodeling. (biomedsearch.com)
  • Vascular proliferation and remodeling are the hallmarks of PH and are found mainly in the pulmonary arterial smooth muscle cells (PASMC). (wku.edu)
  • Recently, our laboratory also found that 20-HETE is involved in promoting prolonged hypoxia-induced pulmonary vasoconstriction and that glucose-6-phosphate dehydrogenase (G6PD), which is a major producer of NADPH in the cell, and cytochrome P -450 monooxygenase enzymes are functionally coupled in vascular smooth muscle tissue (unpublished observations). (physiology.org)
  • Expression of nucleotide-binding oligomerization domain protein 2 (NOD2) is upregulated in pulmonary artery smooth muscle cells (PASMCs) during hypoxia. (oncotarget.com)
  • To investigate the involvement of NOD2 in the pulmonary vascular response to hypoxia, we subjected wild-type and NOD2-deficient mice to chronic normobaric hypoxic conditions. (oncotarget.com)
  • Pulmonary vascular remodeling in NOD2-deficient mice was characterized by increased PASMC proliferation. (oncotarget.com)
  • In vivo studies have indicated that hypoxia increases the wall thickness of pulmonary blood vessels by promoting pulmonary artery smooth muscle cell (PASMC) proliferation [ 4 , 5 ]. (oncotarget.com)
  • Additionally, pulmonary vascular cells have been reported to proliferate in response to hypoxia in vitro [ 6 - 8 ]. (oncotarget.com)
  • The primary emphasis is on the inherent heterogeneity of smooth muscle progenitors and cells and the limitations of current in vitro characterisation. (nih.gov)
  • Vascular smooth muscle cells from the inbred Yucatan minipig were infected in vitro with an amphotropic, replication-defective retrovirus transducing the gene for Escherichia coli beta-galactosidase. (ahajournals.org)
  • calcitonin gene-related peptide and its receptor involve the proliferation and the apoptosis in vivo and in vitro, exogenous receptor activity-modifying protein 1 enhances the antiproliferation effect of calcitonin gene-related peptide in vascular smooth muscle cells. (medicalxpress.com)
  • Akoum, S. , Cloutier, I. and Tanguay, J. (2013) Adipocytes modulate vascular smooth muscle cells migration potential through their secretions. (scirp.org)
  • The physiological role of Rho-specific guanine nucleotide dissociation inhibitor (RhoGDI) in vascular remodeling remains unknown. (bioportfolio.com)
  • Vascular smooth muscle contracts or relaxes to both change the volume of blood vessels and the local blood pressure , a mechanism that is responsible to redistribution of the blood within the body to areas where it is needed (i.e. areas with temporarily enhanced oxygen consumption). (wikidoc.org)
  • Abdominal aortic aneurysm (AAA) is a common vascular disease with, as of yet, unclear mechanism. (ovid.com)
  • A possible interaction between nitric oxide (NO) and the insulin-like growth factor (IGF)-system was studied in cultured rat aortic smooth muscle cells. (diva-portal.org)
  • The interaction of the insulin-like growth factor-system (IGF-system) with various growth factors, glucose and nitric oxide (NO) was studied in vascular cells. (diva-portal.org)
  • Loss of alpha-globin genes in human subjects is associated with improved nitric oxide-mediated vascular perfusion. (onmedica.com)
  • Vascular smooth muscle refers to the particular type of smooth muscle found within, and composing the majority of the wall of blood vessels . (wikidoc.org)
  • Thus the main function of vascular smooth muscle tonus is to regulate the caliber of the blood vessels in the body. (wikidoc.org)
  • Vascular smooth muscle is the type of smooth muscle that makes up most of the walls of blood vessels. (wikipedia.org)
  • Human atheromata, but not normal blood vessels, contain numerous smooth muscle cells (SMC) that bear class II major histocompatibility (MHC) antigens. (harvard.edu)
  • Indeed, Akt activation has been observed during the remodeling of blood vessels and the proliferation of PASMCs following vascular injury and hypoxia [ 10 ], and has been reported to stabilize hypoxia-inducible factor-1 alpha (HIF-1α) [ 11 ]. (oncotarget.com)
  • A chapter that examines the events leading to vascular pathology in the form of atherogenesis concludes the book. (elsevier.com)
  • Interleukin-1 (IL-1) mediates many components of generalized host response to injury and may also contribute to local vascular pathology during immune or inflammatory responses. (harvard.edu)
  • These mice develop progressive loss of vascular smooth muscle cells in the medial layer of large arteries, in a pattern very similar to that seen in children with HGPS. (pnas.org)
  • Because oxidative stress may play a key role in the pathogenesis of diabetic vascular disease, we have examined whether culture of porcine vascular smooth muscle cells (PVSMCs) under high glucose (HG) conditions (25 mmol/l) to simulate the diabetic state can lead to the activation of NF-kappaB, and also whether cytokine- or growth factor-induced NF-kappaB activation is altered by HG culture. (diabetesjournals.org)
  • Since Harman ( 22 ) proposed the original mitochondrial theory of aging, it has been widely accepted that mitochondrial oxidative stress is a major factor in the pathophysiology of aging in many organs, including skeletal muscle, heart, and the brain (reviewed recently elsewhere in Refs. (physiology.org)
  • Treatment of human aortic smooth muscle cells with serum from uremic patients induced osteo-/chondrogenic transdifferentiation, effects ameliorated by EMD638683. (jci.org)
  • Rong, J.X., Shapiro, M., Trogan, E. and Fisher, E.A. (2003) Transdifferentiation of mouse aortic smooth muscle cells to a macrophage-like state after cholesterol loading. (scirp.org)
  • The kinetics of internalization, sequestration and metabolic degradation of atrial natriuretic factor (ANF)-receptor complex were studied in rat thoracic aortic smooth-muscle (RTASM) cells. (portlandpress.com)
  • producing NADH oxidase in cultured rat aortic smooth-muscle cells. (biochemj.org)
  • Here we report the expression of CaSR mRNA and protein (Western blotting and immunocytochemistry) in human aortic smooth muscle cells (HAoSMC) and human arteries (ethical approval obtained). (endocrine-abstracts.org)
  • Hyalinosis is a vascular lesion affecting the renal vasculature and contributing to ageing-related renal function decline. (bioportfolio.com)
  • 20-HETE is proinflammatory and it regulates vascular and renal function ( 49 ). (physiology.org)
  • Corticosterone initiated extracellular signal-regulated kinase 1/2 phosphorylation in rat vascular smooth muscle cells at ≥10 −11 mol/L doses. (ahajournals.org)
  • Mechanical strain of rat vascular smooth muscle cells is sensed by specific extracellular matrix/integrin interactions. (jci.org)
  • Multiple mitogenic stimuli induce vascular SMC proliferation through cell cycle progression. (thefreelibrary.com)
  • Although transplanting mesenchymal stem cells can improve cardiac function and contribute to endothelial recovery in a damaged artery, mesenchymal stem cells may induce neointimal hyperplasia by directly or indirectly acting on vascular smooth muscle cells. (medicalxpress.com)
  • Calcitonin gene related protein (CGRP) is one of the most well-known potent vasodilators and can regulate vascular tone and other aspects of vascular function. (medicalxpress.com)
  • In a search for additional Ca2+ regulatory components in vascular smooth muscle, a novel troponin T-like protein was purified from bovine aorta smooth muscle. (nih.gov)
  • Methods and Results −In this study, we show that LDL increased tissue factor mRNA and cell surface protein in smooth muscle cells without a marked increase in surface tissue factor activity. (ahajournals.org)
  • Many of the remaining DR-positive cells contained the muscle-specific intermediate filament protein, desmin. (unboundmedicine.com)
  • CaSR mRNA and protein was expressed normal arteries (kidney donors) where it was detected in smooth muscle cells and endothelial cells. (endocrine-abstracts.org)
  • 3. The increased sensitivity of vascular smooth muscle after corticosterone treatment is not related to changes in the contractile protein or alterations in the neuronal uptake and extraneuronal metabolism of noradrenaline. (clinsci.org)
  • Actin, alpha skeletal muscle is a protein that in humans is encoded by the ACTA1 gene. (wikipedia.org)
  • Tissue factor expression on the smooth muscle cell surface could be of pathological significance as a contributor to plaque growth, thrombus formation, and the acute coronary syndrome after plaque rupture. (ahajournals.org)
  • M. F. Navedo, Y. Takeda, M. Nieves-Cintrón, J. D. Molkentin, and L. F. Santana, "Elevated Ca2+ sparklet activity during acute hyperglycemia and diabetes in cerebral arterial smooth muscle cells," American Journal of Physiology - Cell Physiology , vol. 298, no. 2, pp. (hindawi.com)
  • No differences were detected between the tissue-specific cGKI mutants and control mice at different time points after vascular injury on a normolipidemic or apoE-deficient background. (nih.gov)
  • Vascular smooth muscle cells from mice deficient in TRPML1 did not generate Ca 2+ sparks, and these mice were spontaneously hypertensive. (sciencemag.org)
  • Furthermore, GlcNAc-Ls were intravenously administered to mice that had undergone wire-mediated vascular injury. (springer.com)
  • Smoothelin-A and -B have only been found in fully differentiated contractile smooth muscle cells. (biomedsearch.com)
  • Recent discoveries on the recruitment of vascular progenitor cells to the sites of vascular injury suggest new therapeutic potentials of progenitor cell-based therapies to accelerate re-endothelialization and prevent engraftment of SMC-lineage progenitor cells. (thefreelibrary.com)
  • A series of pulse-chase experiments revealed that the origin of aortic vascular smooth muscle cells can be traced back to progenitor cells that reside in the wall of the dorsal aorta of the embryo at E10.5. (ovid.com)
  • A distinct population of CD146+ smooth muscle progenitor cells emerges during embryonic development and is maintained postnatally at arterial branch sites. (ovid.com)