View Rat Genome Database annotations to negative regulation of vascular associated smooth muscle cell differentiation involved in phenotypic switching

Osteoprotegerin (tnfsf11b, OPG) is a soluble member of the TNF superfamily originally described as an important regulator of osteoclastogenesis almost 20years ago. OPG is a heparin-binding secreted glycoprotein that exists as a 55-62kDa monomer or a 110-120kDa disulphide-linked homodimer. Acting as a soluble decoy receptor for RANKL, OPG actively regulates RANK signalling, and thereby osteoclastogenesis. OPG has subsequently been shown to also be a decoy receptor TNF related apoptosis inducing-ligand (tnfsf10, TRAIL, Apo2L). TRAIL is a type II transmembrane protein that is widely expressed in a variety of human tissues, including the spleen, lung, and prostate. Through binding to TRAIL, OPG can inhibit TRAIL-induced apoptosis of cancer cells. More recently OPG has been demonstrated to be secreted by, and influence, vascular smooth muscle cells phenotype particularly related to vascular calcification and pulmonary vascular remodelling. In pulmonary artery smooth muscle cell (PASMC) suppression of ...

Endothelial cell signaling in cardiovascular development and disease. Our laboratory helped to establish endoglin functions in non-endothelial cell niches during embryonic development and in adult disease: we established: a functional role for endoglin in vascular smooth muscle cells arising from the neural crest, cell autonomous roles for endoglin in both endothelial and smooth muscle cells of developing blood vessels, and lymphatic vessels.. Tang Y, Urs S, Boucher J, Bernaiche T, Venkatesh D, Spicer DB, Vary CP, Liaw L. Notch and transforming growth factor-beta (TGFbeta) signaling pathways cooperatively regulate vascular smooth muscle cell differentiation. J Biol Chem. 2010;285(23):17556-63. PMCID:2878520.. Mancini ML, Verdi JM, Conley BA, Nicola T, Spicer DB, Oxburgh LH, Vary CP. Endoglin is required for myogenic differentiation potential of neural crest stem cells. Dev Biol. 2007;308(2):520-33. PMCID:2041841.. Mouta-Bellum C, Kirov A, Miceli-Libby L, Mancini ML, Petrova TV, Liaw L, Prudovsky ...

Vascular smooth muscle cell (SMC) differentiation is a very important process during vasculogenesis and angiogenesis, and it is recognized that alterations in S...

Nutrition for Muscle Cell Function. When you think of muscles, you likely think of your skeletal muscle tissue -- the type that attaches to your bones to allow for movement. However, you also have other types of muscle. Cardiac muscle keeps your heart pumping strong, driving your circulation, while the smooth muscle ...

Blirando, K. et al. The stellate vascular smooth muscle cell phenotype is induced by IL-1β via the secretion of PGE2 and subsequent cAMP-dependent protein kinase A activation. Biochim. Biophys. Acta. 1853, 3235-3247 (2015 ...

Principal Investigator：SOBUE Kenji, Project Period (FY)：1995 - 1996, Research Category：Grant-in-Aid for Scientific Research (B), Section：一般, Research Field：General medical chemistry

Muscle cells serve a remarkable variety of functions in your body, many of them occurring involuntarily. The specialized structure of the 3 types of muscle cells in the human body enables their functional purposes.

February 14, 2016 Heart (noun, verb, idioms) heart [hahrt] noun 1. Anatomy. a hollow, pumplike organ of blood circulation, composed mainly of rhythmically contractile smooth muscle, located in the chest between the lungs and slightly to the left and consisting of four chambers: a right atrium that…

muscle cell in human body human coronary artery smooth muscle cells 2 photo, muscle cell in human body human coronary artery smooth muscle cells 2 image, muscle cell in human body human coronary artery smooth muscle cells 2 gallery

TY - JOUR. T1 - Krüppel-like factor 4, Elk-1, and histone deacetylases cooperatively suppress smooth muscle cell differentiation markers in response to oxidized phospholipids. AU - Yoshida, Tadashi. AU - Gan, Qiong. AU - Owens, Gary K.. N1 - Copyright: Copyright 2009 Elsevier B.V., All rights reserved.. PY - 2008/11. Y1 - 2008/11. N2 - Phenotypic switching of vascular smooth muscle cells (SMCs), such as increased proliferation, enhanced migration, and downregulation of SMC differentiation marker genes, is known to play a key role in the development of atherosclerosis. However, the factors and mechanisms controlling this process are not fully understood. We recently showed that oxidized phospholipids, including 1-palmitoyl-2-(5-oxovaleroyl)-sn-glycero-3-phosphocholine (POVPC), which accumulate in atherosclerotic lesions, are potent repressors of expression of SMC differentiation marker genes in cultured SMCs as well as in rat carotid arteries in vivo. Here, we examined the molecular mechanisms ...

TY - JOUR. T1 - Endothelial NO synthase deficiency promotes smooth muscle progenitor cells in association with upregulation of stromal cell-derived factor-1α in a mouse model of carotid artery ligation. AU - Zhang, Le Ning. AU - Wilson, Dennis W. AU - Da Cunha, Valdeci. AU - Sullivan, Mark E.. AU - Vergona, Ronald. AU - Rutledge, John C. AU - Wang, Yi Xin. PY - 2006/4. Y1 - 2006/4. N2 - Background - Endothelial NO deficiency (endothelial NO synthase [eNOS]-knockout [KO]) enhanced smooth muscle cell (SMC)-rich neointimal lesion formation in a mouse model of carotid artery ligation (CAL). Recent evidence indicated that stromal cell-derived factor-1α (SDF-1α)-mediated recruitment of circulating SMC progenitor cells substantially contributed to the SMC-rich neointimal hyperplasia induced by vascular injury. The goal of this study was to investigate the effects of eNOS deficiency on the expression of SDF-1α and mobilization of circulating SMC progenitor cells in CAL model. Methods and Results - ...

Nitric oxide (NO), which is known to inhibit systemic vascular smooth muscle cell proliferation, is used in the management of neonatal pulmonary hypertension. Our objectives were to determine: (1) if endogenous NO production by neonatal porcine pulmonary artery smooth muscle cells (PASMCs) varied with oxygen tension in vitro, and (2) the effect of exogenous NO and inducible NO synthase (iNOS) stimulators and inhibitors on PASMC proliferation and apoptosis. PASMCs were exposed to different conditions (varying PO2, NO donors and scavengers, iNOS stimulators and inhibitors) and proliferation, apoptosis, and cyclic guanosine 5-monophosphate (cGMP) assessed. PASMCs proliferated best between 5 and 10% O2 but cGMP levels were similar at all oxygen levels. NO donors (S-nitroso-N-acetyl-penicillamine, NOC-12, NOC-18) inhibited PASMC proliferation in a dose-dependent manner with associated cGMP increases, while NO scavengers (carboxy-PTIO), iNOS stimulators (interleukin-1β, lipopolysaccharide), and iNOS ...

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 ...

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 ...

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, ...

Cysteine-containing leukotrienes (cysteinyl-LTs) are pivotal inflammatory mediators that play important roles in the pathophysiology of asthma, allergic rhinitis, and other inflammatory conditions. In particular, cysteinyl-LTs exert a variety of effects with relevance to the aetiology of asthma such as smooth muscle contraction, eosinophil recruitment, increased microvascular permeability, enhanced mucus secretion and decreased mucus transport and, finally, airway smooth muscle cells (ASMC) proliferation. We used human ASMC (HASMC) to identify the signal transduction pathway(s) of the leukotriene D4 (LTD4)-induced DNA synthesis. Proliferation of primary HASMC was measured by [3H]thymidine incorporation. Phosphorylation of EGF receptor (EGF-R) and ERK1/2 was assessed with a polyclonal anti-EGF-R or anti-phosphoERKl/2 monoclonal antibody. A Ras pull-down assay kit was used to evaluate Ras activation. The production of reactive oxygen species (ROS) was estimated by measuring dichlorodihydrofluorescein (DCF

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 ...

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 ...

DCU ConnectedconnectedWhat if you could work towards a world-class online Irish University degree on your own schedule, from the comfort of your own home, in your own town, in any place in the world? Online learning with DCU Connected gives you remote access to all the resources of an established university: an innovative curriculum, renowned teachers and lively exchange with your fellow learners.

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 ...

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 ...

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. ...

Maspin is a serpin that has multiple effects on cell behavior, including inhibition of migration. How maspin mediates these diverse effects remains unclear, as it is devoid of protease inhibitory activity. We have previously shown that maspin rapidly inhibits the migration of vascular smooth muscle cells (VSMC), suggesting the involvement of direct interactions with cell surface proteins. Here, using immunofluorescence microscopy, we demonstrate that maspin binds specifically to the surface of VSMC in the dedifferentiated, but not the differentiated, phenotype. Ligand blotting of VSMC lysates revealed the presence of several maspin-binding proteins, with a protein of 150 kDa differentially expressed between the two VSMC phenotypes. Western blotting suggested that this protein was the beta1 integrin subunit, and subsequently both alpha3beta1 and alpha5beta1, but not alphavbeta3, were shown to associate with maspin by coimmunoprecipitation. Specific binding of these integrins was also observed ...

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 ...

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. ...

Actin, Muscle Specific (Muscle Cell Marker) Antibody, Mouse Monoclonal Antibody [Clone HHF35 + MSA/953 ] validated in IHC-P, IF, FC (AH13010-7), Abgent

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 ...

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 ...

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

Vascular smooth muscle cell (SMC) migration and proliferation are regulated by signaling through the Rho family GTPases, RhoA and Rac, which are activated by GTP exchange factors (GEFs). One such Rho-GEF was recently associated with human atherosclerosis by genetic epidemiology: kalirin, a 340 kDa protein containing both Rac- and RhoA-GEF domains. We tested the hypothesis that SMC kalirin promotes Rac or RhoA signaling, and thereby atherogenic SMC activity. By immunoblotting (IB) and quantitative immunofluorescence microscopy, we found that kalirin is expressed abundantly in SMCs, and is up-regulated 1.6±0.2-fold (p,0.03) in the media of atherosclerotic, as compared with normal arteries. To test kalirins role in regulating SMC signaling, we compared 3 independent lines of SMCs from congenic WT and kalirin−/+ mice (with 45±5% of WT kalirin levels), as well as SMCs transfected with non-targeting or kalirin-targeting siRNA (43±9% protein knockdown). We assessed Rac and RhoA activation by ...

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 ...

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.

Antibodies for proteins involved in positive regulation of smooth muscle cell differentiation pathways, according to their Panther/Gene Ontology Classification

Coronary artery bypass grafting using autologous saphenous veins is a standard surgical therapy for coronary artery diseases. However, post-procedure vein graft restenosis impedes its effectiveness and often leads to a high morbidity and mortality, and a reduction in the quality of life. Neointimal …

To isolate specific markers of both differentiated and proliferating vascular smooth muscle cells (VSMCs), we used the technique of differential cDNA screening using RNA from cultured rat aortic VSMCs. The tissue specificity of expression of all of the cDNAs isolated was determined by Northern analysis. We isolated seven distinct cDNAs that were more strongly expressed in freshly dispersed, differentiated, aortic VSMCs compared with dedifferentiated late-passage cells. These were the cDNAs for tropoelastin, a matrix protein; alpha-smooth muscle (SM) actin, gamma-SM actin, calponin, and phospholamban, which are all proteins associated with the contractile function of differentiated VSMCs; SM22 alpha, a smooth muscle-specific protein of unknown function, and CHIP28, a putative membrane channel protein that is not highly expressed in other SM tissues and may therefore be a new VSMC marker. Two cDNAs that were expressed preferentially in late-passage dedifferentiated VSMCs were also isolated. These ...

OBJECTIVE: Cerebral aneurysm is a common vascular disease with high morbidity and mortality. Vascular smooth muscle deletion or dysplasia is an important r

Fingerprint Dive into the research topics of Angiotensin II enhances AT ,sub,1,/sub,-Nox1 binding and stimulates arterial smooth muscle cell migration and proliferation through AT ,sub,1,/sub,, Nox1, and interleukin-18. Together they form a unique fingerprint. ...

TY - JOUR. T1 - Original Research. T2 - Role of phosphodiesterases in modulation of BK Ca channels in hypertensive pulmonary arterial smooth muscle. AU - Zhu, Shu. AU - White, Richard E.. AU - Barman, Scott A. PY - 2008/1/1. Y1 - 2008/1/1. N2 - BK Ca channels regulate pulmonary arterial pressure, and protein kinase C (PKC) inhibits BK Ca channels, but little is known about PKC-mediated modulation of BK Ca channel activity in pulmonary arterial smooth muscle. Studies were carried out to determine mechanisms of PKC modulation of BK Ca channel activity in pulmonary arterial smooth muscle cells (PASMC) of the fawn-hooded rat (FHR), an animal model of pulmonary hypertension. Forskolin opened BK Ca channels in FHR PASMC, which was blocked by PKC activation, and reversed by the phosphodiesterase (PDE) inhibitors IBMX, milrinone, and zaprinast. PDE inhibition also blocked the vasoconstrictor response to PKC activation in FHR pulmonary arteries. These results indicate that PKC inhibits cAMP-induced ...

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 - ...

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. ...

Serum response factor (SRF) controls [smooth muscle cell] SMC gene transcription via binding to CArG box DNA sequences found within genes that exhibit SMC-restricted expression.[2] SMC genes examined in this study display SMC-specific histone modifications at the 5′-CArG boxes.[2] The SRF-CArG association is required for transcriptional activation of SMC genes [...] the SMC genes examined in this study display SMC-specific histone modifications at the 5′-CArG boxes. [...] enrichment of H4 and H3 acetylation [...] were relatively low from positions -2,800 to -1,600 in the 5′ region. However, at position -1,600 to -1,200, there was a sharp rise in these modifications, which was increased even further at +400 in the coding region. We observed similar patterns for H3K4dMe and H3 Lys79 di-methylation [...]. SRF, TFIID, and RNA polymerase II displayed enrichments that were consistent with the positions of the CArG boxes, TATA box, and coding region, respectively.[2] The CArG boxes occur ...

Histone deacetylases (HDACs) are transcriptional coregulators. Recently, we demonstrated that HDAC4, one of class IIa family members, promotes reactive oxygen species-dependent vascular smooth muscle inflammation and mediates development of hypertension in spontaneously hypertensive rats. Pathogenesis of hypertension is, in part, modulated by vascular structural remodeling via proliferation and migration of vascular smooth muscle cells (SMCs). Thus, we examined whether HDAC4 controls SMC proliferation and migration. In rat mesenteric arterial SMCs, small interfering RNA against HDAC4 inhibited platelet-derived growth factor (PDGF)-BB-induced SMC proliferation as determined by a cell counting and bromodeoxyuridine incorporation assay as well as migration as determined by Boyden chamber assay. Expression and activity of HDAC4 were increased by PDGF-BB. HDAC4 small interfering RNA inhibited phosphorylation of p38 mitogen-activated protein kinase and heat shock protein 27 and expression of cyclin D1 ...

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 ...

The relationship between aging and restenosis are unclear. The purposes of this study were to investigate the possible pathological role and mechanism of aging on formation of restenosis. Our data indicated that cell proliferation and migration of the oxidative stress-induced senescent vascular smooth muscle cells were obviously desensitized to stimulation by platelet-derived growth factor (PDGF)-BB, which may have been caused by suppression of promoter activity, transcription, translation, and activation levels of PDGF receptor (PDGFR)-β. The analyzed data obtained from the binding array of transcription factors (TFs) showed that binding levels of eighteen TFs on the PDGFR-β promoter region (-523 to -1) were significantly lower in senescent cells compared to those of non-senescent cells. Among these TFs, the bioinformatics prediction suggested that the putative binding sites of ten TFs were found in this promoter region. Of these, transcriptional levels of seven TFs were markedly reduced in

Vascular smooth muscle cell (VSMC) viability and homeostasis is regulated by cell-matrix and cell-cell contact: disruption of these interactions are responsible of a switch from a mature to a high proliferative phenotype. VSMCs migration, rate of growth and apoptosis, and the extent of their extracellular matrix (ECM) deposition can be also modulated by proatherogenic peptides. Among them, ATII induces the transactivation of IGF I R, which, together with the binding protein IGFBP3, represents a determinant of cell survival, growth and proliferation. Aim of our in vitro study was to verify the role of elective cell-cell bond in moulating the response to ATII. Thus, we evaluated viability, proliferation, IGFIR, IGFBP3 expression and the long term survival and production of ECM in a provisional tissue. A7r5 cell-line was used in adherent cultures or incubated in agarose-coated culture plates to inhibit cell-matrix interactions. Cells, treated or not with ATII 100 nM, were evaluated for apoptosis ...

Apoptosis of vascular smooth muscle cells induces features of plaque vulnerability in atherosclerosis. Connexin37 protects against atherosclerosis by regulating monocyte adhesion

TY - CONF. T1 - Import and signaling of oxidized phospholipids in vascular smooth muscle cells. AU - Hermetter, Albin. AU - Loidl, Alexandra. AU - Morak, Maria. AU - Moumtzi, Alexandra. AU - Trenker, Michael. PY - 2006/6/16. Y1 - 2006/6/16. M3 - (Old data) Lecture or Presentation. T2 - HNE-Club Meeting. Y2 - 16 June 2006 through 18 June 2006. ER - ...

The Microcirculatory Core Laboratorys primary mission is to study regulation of cardiovascular resistance at the vascular level. Our experties contribute to the mission of the Consortium for Integrative Cardiovascular Research by providing a intermediate level of investigation between integrative (intact animal and whole organ) and vascular biology (isolated endothelial and vascular smooth muscle cell) studies.. Research Interests The Microcirculatory Core Laboratory specialises in isolated vascular preparations to study intrinsic regulation of vascular tone. We are interested in endothelial and smooth muscle cell function in health and disease. We predominantly study resistance vessels (arterioles and small arteries), since these are primary determinants of resistance in the cardiovascular circuit. We use disease models where resistance vascular function is altered, such as experimental models of hemorrhagic shock, hypertension, obesity, insulin resistance, and diabetes. ...

In this study, we demonstrated that Bo-Gan-Whan (BGH), a Korean polyherbal medicine, has an inhibitory effect on VSMC migration and proliferation in response to PDGF-BB as revealed by the results obtained from the scratch-wound healing and Boyden chamber assay and sprout aortic ring assays, respectively. Moreover, it was demonstrated through western blot analysis that the modulation of MAPKs is the major signal that is activated in the pathogenesis of VSMCs through activation of the ERK1/2 and p38 MAPK pathways. These results were confirmed from the ex vivo analysis of PDGF-BB-induced VSMCs migration and proliferation. The data on ex vivo analysis, through outgrowth of vessel sprouts from the aortic strips assay, show that BGH treatment can significantly reduce VSMC migration and proliferation after PDGF-BB stimulation.. Abnormal proliferation of VSMCs is a key to the vascular pathological conditions such as atherosclerosis and restenosis. Moreover, excessive migration of VSMCs in vascular ...

By Andrew R Bond, Dominga Iacobazzi, Safa Abdul-Ghani, Mohammed Ghorbel, Kate Heesom, Mariangela Wilson, Christopher Gillett, Sarah J George, Massimo Caputo, Saadeh Suleiman and Robert M R Tulloh ...

Pyne, Nigel and Pyne, Susan; Giembycz, M and Raeburn, D, eds. (1994) G-proteins in airway smooth muscle. In: Airways Smooth Muscle. Birkhauser Velaag, pp. 187-213. ISBN 9780817650438 Full text not available in this repository.Request a copy from the Strathclyde author ...

In vertebrates, gut coiling proceeds left-right asymmetrically throughout growth of the gastrointestinal tract with extremely organized muscular buildings facilitating peristalsis. In this report, we explored the mechanisms of larval gut coiling morphogenesis related to its nascent smooth muscle cells utilizing extremely clear Xenopus early larvae.. First, to visualise the dynamics of intestinal smooth muscle cells, whole-mount specimens had been immunostained with anti-smooth muscle-specific actin (SM-actin) antibody. We discovered that the nascent gut of Xenopus early larvae steadily expands the SM-actin-positive area in a stage-dependent method. Transverse orientation of smooth muscle cells was first established, and subsequent, the mobile longitudinal orientation alongside the gut axis was adopted to make a meshwork of the contractile cells.. Finally, anisotropic torsion by the smooth muscle cells was generated in the heart of gut coiling, suggesting that twisting drive may be concerned in ...

In vertebrates, gut coiling proceeds left-right asymmetrically throughout growth of the gastrointestinal tract with extremely organized muscular buildings facilitating peristalsis. In this report, we explored the mechanisms of larval gut coiling morphogenesis related to its nascent smooth muscle cells utilizing extremely clear Xenopus early larvae.. First, to visualise the dynamics of intestinal smooth muscle cells, whole-mount specimens had been immunostained with anti-smooth muscle-specific actin (SM-actin) antibody. We discovered that the nascent gut of Xenopus early larvae steadily expands the SM-actin-positive area in a stage-dependent method. Transverse orientation of smooth muscle cells was first established, and subsequent, the mobile longitudinal orientation alongside the gut axis was adopted to make a meshwork of the contractile cells.. Finally, anisotropic torsion by the smooth muscle cells was generated in the heart of gut coiling, suggesting that twisting drive may be concerned in ...

In the current study in T2DM patients, indices of vascular function were found to be inter-related suggesting that they probably reflect overlapping pathophysiological aspects of the vascular atherosclerotic damage in T2DM patients. Further to this finding, markers of endothelial function (FMD), smooth muscle cell function (NMD) and large artery stiffness (PWV) were shown to share common correlates. Older age, longer duration of diabetes and treatment with insulin were associated with all markers of vascular dysfunction, although each marker appeared to be independently associated with specific distinct parameters.. Previous studies comparing patients with T2DM to healthy controls have shown that T2DM is an independent risk factor for endothelial dysfunction [14, 16, 17]. The greater cardiovascular mortality risk observed in T2DM patients has been mainly attributed to vascular endothelial dysfunction [17]. In T2DM patients without macrovascular or microvascular disease, we found that endothelial ...