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 - The effect of anti-hypertensive drugs on DNA synthesis and proliferation of cultured rat aortic smooth muscle cells. AU - Kang, Shin Wook. AU - Lee, In Hee. AU - Choi, Kyu Hun. AU - Lee, Ho Yung. AU - Han, Dae Suk. PY - 1997. Y1 - 1997. N2 - The aim of this study was to elucidate the effects of anti-hypertensive drugs, nifedipine, furosemide, hydrochlorothiazide, captopril, and atenolol on DNA synthesis and proliferation of cultured rat aortic smooth muscle cells induced by fetal calf serum. Aortic smooth muscle cells from Sprague-Dawley rats were isolated, cultured, and seeded in multi-well plates. When confluent, cells were cultured in a conditioned medium without fetal calf serum. After 72 hours, cells were cultured in the medium retaining 10% fetal calf serum with or without anti-hypertensive drugs by increasing the concentration between 10-8 and 10-4M. DNA synthesis was assessed by [3H]-thymidine uptake and proliferation by cell numbers using a hemocytometer. Nifedipine at a ...
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 ...
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
The bacteriolysin lysostaphin (Lst) and endolysin PlyPH are potent modular lytic enzymes with exercise in opposition to clinically-relevant Gram-positive Staphylococcus aureus and Bacillus cereus, respectively. Both enzymes possess an N-terminal catalytic area and C-terminal binding area, with the latter conferring important enzyme specificity. Lst and PlyPH present diminished exercise within the presence of bacterial growth-supporting …. Influence of Bacterial Culture Medium on Peptidoglycan Binding of Cell Wall Lytic Enzymes Read More ». ...
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