983 results match your criteria vsmcs enhanced

Oxidant-Resistant LRRC8A/C anion channels support superoxide production by Nox1.

J Physiol 2021 May 1. Epub 2021 May 1.

Department of Pediatrics, Vanderbilt University Medical Center, Nashville, TN, 37232, United States.

Key Points: LRRC8A-containing anion channels associate with Nox1 and regulate superoxide production and TNFα signaling. Here we show that LRRC8C and 8D also co-immunoprecipitate with Nox1 in vascular smooth muscle cells. LRRC8C knockdown inhibited TNFα-induced O production, receptor endocytosis, NF-κB activation, and proliferation while LRRC8D knockdown enhanced NF-κB activation. Read More

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Nkx2-3 induces autophagy inhibiting proliferation and migration of vascular smooth muscle cells via AMPK/mTOR signaling pathway.

J Cell Physiol 2021 Apr 30. Epub 2021 Apr 30.

Department of Cardiology, Laboratory of Heart Center, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong, China.

Vascular remodeling and restenosis are common complications after percutaneous coronary intervention. Excessive proliferation and migration of vascular smooth muscle cells (VSMCs) play important roles in intimal hyperplasia-induced vascular restenosis. NK2 Homeobox 3 (Nkx2-3), a critical member of Nkx family, is involved in tissue differentiation and organ development. Read More

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LINC01278 Sponges miR-500b-5p to Regulate the Expression of ACTG2 to Control Phenotypic Switching in Human Vascular Smooth Muscle Cells During Aortic Dissection.

J Am Heart Assoc 2021 May 29;10(9):e018062. Epub 2021 Apr 29.

Department of Cardiovascular Surgery of the Second Hospital of Jilin University Changchun Jilin China.

Background Phenotypic switching in vascular smooth muscle cells (VSMCs) is involved in the pathogenesis of aortic dissection (AD). This study aims to explore the potential mechanisms of linc01278 during VSMC phenotypic switching. Methods and Results Twelve samples (6 AD and 6 control) were used for lncRNA, microRNA, and mRNA microarray analysis. Read More

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Oleic acid induces A7r5 cell proliferation and migration associated with increased expression of HGF and p‑p38.

Mol Med Rep 2021 Jul 28;24(1). Epub 2021 Apr 28.

Laboratory of Disorders Genes and Department of Pharmacology, Jishou University School of Pharmacy, Jishou, Hunan 416000, P.R. China.

The phenotypes and mechanisms underlying the proliferation and migration of vascular smooth muscle cells (VSMCs) induced by oleic acid (OA) are not completely understood. Therefore, the aim of the present study was to further elucidate the effects of OA on the proliferation and migration of VSMCs. Using A7r5 cells, the hepatocyte growth factor (HGF) inhibitor PHA665752 and the p38 MAPK inhibitor SB203580 were utilized, and Cell Counting Kit‑8 (CCK‑8) assays, Transwell assays, flow cytometry, ELISAs, western blotting and reverse transcription‑quantitative PCR (RT‑qPCR) were conducted to assess the effects of OA. Read More

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SM22 Loss Contributes to Apoptosis of Vascular Smooth Muscle Cells via Macrophage-Derived circRasGEF1B.

Oxid Med Cell Longev 2021 16;2021:5564884. Epub 2021 Mar 16.

Department of Biochemistry and Molecular Biology, College of Basic Medicine, Key Laboratory of Medical Biotechnology of Hebei Province, Hebei Medical University, Shijiazhuang, Hebei 050017, China.

Vascular smooth muscle cell (VSMC) apoptosis is a major defining feature of abdominal aortic aneurysm (AAA) and mainly caused by inflammatory cell infiltration. Smooth muscle (SM) 22 prevents AAA formation through suppressing NF-B activation. However, the role of SM22 in VSMC apoptosis is controversial. Read More

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Circular RNA circ-ARFIP2 regulates proliferation, migration and invasion in human vascular smooth muscle cells via miR-338-3p-dependent modulation of KDR.

Metab Brain Dis 2021 Apr 10. Epub 2021 Apr 10.

Department of Neurosurgery, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, No.106 Zhongshan Second Road, Guangzhou, 510000, Guangdong, China.

Dysfunction of vascular smooth muscle cells (VSMCs) plays a critical role in the pathogenesis of intracranial aneurysm (IA). Circular RNAs (circRNAs) have been implicated in the pathogenesis of IA by reducing microRNA (miRNA) activity. In this paper, we investigated the precise roles of circRNA ADP ribosylation factor interacting protein 2 (circ-ARFIP2, circ_0021001) in VSMC dysfunction. Read More

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Sodium Selenite Attenuates Balloon Injury-Induced and Monocrotaline-Induced Vascular Remodeling in Rats.

Front Pharmacol 2021 15;12:618493. Epub 2021 Mar 15.

Department of Cardiology, Lishui Hospital of Zhejiang University, The Fifth Affiliated Hospital of Wenzhou Medical University, Lishui Municipal Central Hospital, Lishui, China.

Vascular remodeling (VR), induced by the massive proliferation and reduced apoptosis of vascular smooth muscle cells (VSMCs), is primarily responsible for many cardiovascular conditions, such as restenosis and pulmonary arterial hypertension. Sodium selenite (SSE) is an inorganic selenium, which can block proliferation and stimulate apoptosis of tumor cells; still, its protective effects on VR remains unknown. In this study, we established rat models with carotid artery balloon injury and monocrotaline induced pulmonary arterial hypertension and administered them SSE (0. Read More

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Thymosin β4 protects against aortic aneurysm via endocytic regulation of growth factor signaling.

J Clin Invest 2021 Mar 30. Epub 2021 Mar 30.

Department of Physiology, Anatomy, and Genetics, University of Oxford, Oxford, United Kingdom.

Vascular stability and tone are maintained by contractile smooth muscle cells (VSMCs). However, injury-induced growth factors stimulate a contractile-synthetic phenotypic modulation which increases susceptibility to abdominal aortic aneurysm (AAA). As a regulator of embryonic VSMC differentiation, we hypothesised that Thymosin β4 (Tβ4) may function to maintain healthy vasculature throughout postnatal life. Read More

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Sitagliptin, a dipeptidyl peptidase-4 inhibitor, attenuates apoptosis of vascular smooth muscle cells and reduces atherosclerosis in diabetic apolipoprotein E-deficient mice.

Vascul Pharmacol 2021 Mar 26:106854. Epub 2021 Mar 26.

Department of Cardiology, Chinese Hainan Hospital of PLA General Hospital, Sanya, Hainan Province, China.

Sitagliptin, a dipeptidyl peptidase-4(DPP-4) Inhibitor, has been found to have an anti-atherosclerotic effect. Since apoptosis of vascular smooth muscle cells (VSMCs) contributes to the occurrence of diabetic atherosclerosis. This study aimed to examine whether sitagliptin suppresses the atherosclerosis progression to hyperglycemia in a low-dose streptozotocin (STZ)-induced diabetic mouse model, and then investigated the effect of sitagliptin on VSMCs apoptosis and its underlying mechanism. Read More

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LncRNA AC105942.1 Downregulates hnRNPA2/B1 to Attenuate Vascular Smooth Muscle Cells Proliferation.

DNA Cell Biol 2021 May 30;40(5):652-661. Epub 2021 Mar 30.

Department of Laboratory Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China.

The abnormal proliferation of vascular smooth muscle cells (VSMCs) is crucial in the atherosclerosis. Although long noncoding RNAs (lncRNAs) are implicated in a variety of diseases, their roles in activation of VSMCs proliferation and vascular disorder diseases are not well understood. In addition, heterogeneous nuclear ribonucleoprotein A2/B1 (hnRNPA2/B1) was reported to participate in lncRNAs-mediated function. Read More

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Mitochondrial Oxidative Stress Enhances Vasoconstriction by Altering Calcium Homeostasis in Cerebrovascular Smooth Muscle Cells under Simulated Microgravity.

Biomed Environ Sci 2021 Mar;34(3):203-212

Department of Cardiovascular Medicine, Chinese PLA General Hospital & Chinese PLA Medical School, Beijing 100853, China.

Objective: Exposure to microgravity results in postflight cardiovascular deconditioning in astronauts. Vascular oxidative stress injury and mitochondrial dysfunction have been reported during this process. To elucidate the mechanism for this condition, we investigated whether mitochondrial oxidative stress regulates calcium homeostasis and vasoconstriction in hindlimb unweighted (HU) rat cerebral arteries. Read More

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miR‑541‑3p inhibits the viability and migration of vascular smooth muscle cells via targeting STIM1.

Mol Med Rep 2021 May 24;23(5). Epub 2021 Mar 24.

Department of Cardiology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, P.R. China.

The transformation of vascular smooth muscle cells (VSMCs) into the proliferative migratory phenotype in the plaque area contributes to stable plaque formation and facilitates the pathogenesis of atherosclerosis. Stromal interaction molecule 1 (STIM1) has been identified to promote the proliferation of VSMCs, suggesting that STIM1 may be a potent target for the prevention and treatment of atherosclerosis. Bioinformatics analysis has previously predicted STIM1 as a target of microRNA (miR)‑541‑3p. Read More

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Anxa1 in smooth muscle cells protects against acute aortic dissection.

Cardiovasc Res 2021 Mar 23. Epub 2021 Mar 23.

The Institute of Cardiovascular Sciences and Institute of Systems Biomedicine, School of Basic Medical Sciences, Peking University Health Science Center, Key Laboratory of Molecular Cardiovascular Science of Ministry of Education, Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides of Ministry of Health, Beijing Key Laboratory of Cardiovascular Receptors Research, Beijing, 100191, China.

Aims: Acute aortic dissection (AAD) is a life-threatening disease with high morbidity and mortality. Previous studies have showed that vascular smooth muscle cell (VSMC) phenotype switching modulates vascular function and AAD progression. However, whether an endogenous signaling system that protects AAD progression exists, remains unknown. Read More

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20-HETE-promoted cerebral blood flow autoregulation is associated with enhanced pericyte contractility.

Prostaglandins Other Lipid Mediat 2021 Mar 19;154:106548. Epub 2021 Mar 19.

Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, MS, 39216, USA. Electronic address:

We previously reported that deficiency in 20-HETE or CYP4A impaired the myogenic response and autoregulation of cerebral blood flow (CBF) in rats. The present study demonstrated that CYP4A was coexpressed with alpha-smooth muscle actin (α-SMA) in vascular smooth muscle cells (VSMCs) and most pericytes along parenchymal arteries (PAs) isolated from SD rats. Cell contractile capabilities of cerebral VSMCs and pericytes were reduced with a 20-HETE synthesis inhibitor, HET0016, but restored with 20-HETE analog WIT003. Read More

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Glutamine switches vascular smooth muscle cells to synthetic phenotype through inhibiting miR-143 expression and upregulating THY1 expression.

Life Sci 2021 Mar 16:119365. Epub 2021 Mar 16.

Department of Cardiovascular Medicine, The Second Affiliated Hospital of Xi'an Jiaotong University, 157 Xi Wu Road, 710004 Xi'an, China. Electronic address:

Aims: Vascular smooth muscle cells (VSMCs) are involved in the pathogenesis of many human cardiovascular diseases. They modulate their phenotype from "contractile" to "synthetic" in response to changes in local environmental cues. How glutamine regulates the differentiation of VSMCs and the underlying mechanisms remain largely unknown. Read More

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High-mobility group box-1 promotes vascular calcification in diabetic mice via endoplasmic reticulum stress.

J Cell Mol Med 2021 Apr 16;25(8):3724-3734. Epub 2021 Mar 16.

Department of Cardiology, Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medical School, Nanjing, China.

Several studies reported the role of endoplasmic reticulum stress (ERS) in vascular calcification. High-mobility group box-1 (HMGB-1) plays a substantial role in diabetes and its complications. However, relatively little information is available regarding the association between HMGB-1 and calcification, and the underlying mechanism has still remained elusive. Read More

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Mitochondrial Damage-Induced Innate Immune Activation in Vascular Smooth Muscle Cells Promotes Chronic Kidney Disease-Associated Plaque Vulnerability.

Adv Sci (Weinh) 2021 Mar 6;8(5):2002738. Epub 2021 Jan 6.

Department of Nephrology the Key Laboratory for the Prevention and Treatment of Chronic Kidney Disease of Chongqing Kidney Center of PLA Xinqiao Hospital Army Medical University (Third Military Medical University) Chongqing 400037 China.

Chronic kidney disease (CKD) is associated with accelerated atherosclerosis progression and high incidence of cardiovascular events, hinting that atherosclerotic plaques in CKD may be vulnerable. However, its cause and mechanism remain obscure. Here, it is shown that apolipoprotein E-deficient (ApoE) mouse with CKD (CKD/ApoE mouse) is a useful model for investigating the pathogenesis of plaque vulnerability, and premature senescence and phenotypic switching of vascular smooth muscle cells (VSMCs) contributes to CKD-associated plaque vulnerability. Read More

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RTEF-1 Inhibits Vascular Smooth Muscle Cell Calcification through Regulating Wnt/β-Catenin Signaling Pathway.

Calcif Tissue Int 2021 Mar 13. Epub 2021 Mar 13.

Department of Geriatrics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jiefang Avenue, Wuhan, 430022, Hubei, China.

Vascular calcification (VC) is highly prevailing in cardiovascular disease, diabetes mellitus, and chronic kidney disease and, when present, is associated with cardiovascular events and mortality. The osteogenic differentiation of vascular smooth muscle cells (VSMCs) is regarded as the foundation for mediating VC. Related transcriptional enhancer factor (RTEF-1), also named as transcriptional enhanced associate domain (TEAD) 4 or transcriptional enhancer factor-3 (TEF-3), is a nuclear transcriptional factor with a potent effect on cardiovascular diseases, apart from its oncogenic role in the canonical Hippo pathway. Read More

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Sirt7 Deficiency Attenuates Neointimal Formation Following Vascular Injury by Modulating Vascular Smooth Muscle Cell Proliferation.

Circ J 2021 Mar 5. Epub 2021 Mar 5.

Department of Cardiovascular Medicine, Faculty of Life Sciences, Kumamoto University.

Background: Sirt7 is a recently identified sirtuin and has important roles in various pathological conditions, including cancer progression and metabolic disorders. It has previously been reported that Sirt7 is a key molecule in acute myocardial wound healing and pressure overload-induced cardiac hypertrophy. In this study, the role of Sirt7 in neointimal formation after vascular injury is investigated. Read More

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MicroRNA-194 acts as a suppressor during abdominal aortic aneurysm via inhibition of KDM3A-mediated BNIP3.

Life Sci 2021 Mar 1;277:119309. Epub 2021 Mar 1.

Department of Vascular Surgery, The First Hospital of Jilin University, Changchun 130021, PR China. Electronic address:

Aims: Abdominal aortic aneurysm (AAA) is a serious disorder with a high disability rates and mortality rates. Accumulating evidence has identified the vital functions of microRNAs (miRNAs) in the treatment of AAA. Hence, this study is aimed at exploring the modulatory role of miR-194 in the development of AAA. Read More

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Inhibition of miR-135a-5p attenuates vascular smooth muscle cell proliferation and vascular remodeling in hypertensive rats.

Acta Pharmacol Sin 2021 Feb 15. Epub 2021 Feb 15.

Department of Physiology, Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center of Translational Medicine for Cardiovascular Disease, Nanjing Medical University, Nanjing, 211166, China.

Proliferation of vascular smooth muscle cells (VSMCs) greatly contributes to vascular remodeling in hypertension. This study is to determine the roles and mechanisms of miR-135a-5p intervention in attenuating VSMC proliferation and vascular remodeling in spontaneously hypertensive rats (SHRs). MiR-135a-5p level was raised, while fibronectin type III domain-containing 5 (FNDC5) mRNA and protein expressions were reduced in VSMCs of SHRs compared with those of Wistar-Kyoto rats (WKYs). Read More

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February 2021

K 1.3 channels are novel determinants of macrophage-dependent endothelial dysfunction in angiotensin II-induced hypertension in mice.

Br J Pharmacol 2021 Apr 1;178(8):1836-1854. Epub 2021 Mar 1.

Departamento de Farmacología, Universidad Autónoma de Madrid, Instituto de Investigación Hospital La Paz, Madrid, Spain.

Background And Purpose: K 1.3 channels are expressed in vascular smooth muscle cells (VSMCs), where they contribute to proliferation rather than contraction and participate in vascular remodelling. K 1. Read More

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Modulation of Vascular Smooth Muscle Cell Phenotype by High Mobility Group AT-Hook 1.

J Lipid Atheroscler 2021 Jan 13;10(1):99-110. Epub 2021 Jan 13.

Gene and Cell Therapy Center for Vessel-Associated Disease, Medical Research Institute, and Department of Pharmacology, Pusan National University School of Medicine, Yangsan, Korea.

Objective: The purpose of this study is to examine the effect of high mobility group AT-hook 1 (HMGA1) on the phenotyptic change of vascular smooth muscle cells (VSMCs).

Methods: Gene silencing and overexpression of HMGA1 were introduced to evaluate the effect of HMGA1 expression on the phenotypic change of VSMCs. Marker gene expression of VSMCs was measured by promoter assay, quantitative polymerase chain reaction, and western blot analysis. Read More

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January 2021

Zingerone Attenuates Pi-induced Vascular Calcification via AMPK-mediated TIMP4 Expression.

J Lipid Atheroscler 2021 Jan 3;10(1):62-73. Epub 2020 Nov 3.

Department of Biotechnology, College of Engineering, Daegu University, Gyeongsan, Korea.

Objective: Vascular calcification requires the differentiation of vascular smooth muscle cells (VSMCs) into osteoblast-like cells. This phenomenon can be enhanced by inflammation and oxidative stress. Zingerone is one of the active ingredients present in the ginger plant that has anti-inflammatory and antioxidant effects. Read More

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January 2021

TLR4 regulates vascular smooth muscle cell proliferation in hypertension via modulation of the NLRP3 inflammasome.

Am J Transl Res 2021 15;13(1):314-325. Epub 2021 Jan 15.

Department of Nephrology, The First Hospital of China Medical University Shenyang, China.

Backgroud: Toll-like receptor 4 (TLR4), a key mediator of inflammatory responses, which is associated with vascular remodeling. The association between TLR4 and NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome in the regulation of vascular smooth muscle cell (VSMC) proliferation remains unclear. This study was to explore the role and underlying mechanisms of TLR4 in the proliferation of VSMC in hypertension. Read More

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January 2021

Bioinformatics Analysis Reveals MicroRNA-193a-3p Regulates ACTG2 to Control Phenotype Switch in Human Vascular Smooth Muscle Cells.

Front Genet 2020 12;11:572707. Epub 2021 Jan 12.

Department of Cardiovascular Surgery of the Second Hospital of Jilin University, The Second Hospital of Jilin University, Changchun, China.

Aortic dissection (AD) is among the most fatal cardiovascular diseases. However, the pathogenesis of AD remains poorly understood. This study aims to integrate the microRNAs (miRNA) and mRNA profiles and use bioinformatics analyses with techniques in molecular biology to delineate the potential mechanisms involved in the development of AD. Read More

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January 2021

Resistin-like molecule beta augments phenotypic modulation of human aortic smooth muscle cell triggered by high glucose.

Endocr J 2021 Apr 13;68(4):461-468. Epub 2021 Jan 13.

Department of Endocrinology, Huashan Hospital, Fudan University, Shanghai 200040, China.

Vascular muscle cells (VSMCs) participate in the pathophysiology of atherosclerosis. Resistin-like molecule beta (Relmβ) contributes to atherosclerosis development by activating macrophage. This study aims to investigate whether Relmβ regulates VSMC phenotypic modulation under high glucose environment. Read More

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Reversal of Endothelial Extracellular Vesicle-Induced Smooth Muscle Phenotype Transition by Hypercholesterolemia Stimulation: Role of NLRP3 Inflammasome Activation.

Front Cell Dev Biol 2020 21;8:597423. Epub 2020 Dec 21.

Department of Pharmacology and Toxicology, School of Medicine, Virginia Commonwealth University, Richmond, VA, United States.

Recent studies reported that vascular endothelial cells (ECs) secrete NLR family pyrin domain-containing 3 (NLRP3) inflammasome products such as interleukin-1β (IL-1β) via extracellular vesicles (EVs) under various pathological conditions. EVs represent one of the critical mechanisms mediating the cell-to-cell communication between ECs and vascular smooth muscle cells (VSMCs). However, whether or not the inflammasome-dependent EVs directly participate in the regulation of VSMC function remains unknown. Read More

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December 2020

Cyclic Stretch Induces Vascular Smooth Muscle Cells to Secrete Connective Tissue Growth Factor and Promote Endothelial Progenitor Cell Differentiation and Angiogenesis.

Front Cell Dev Biol 2020 9;8:606989. Epub 2020 Dec 9.

School of Life Sciences and Biotechnology, Institute of Mechanobiology and Medical Engineering, Shanghai Jiao Tong University, Shanghai, China.

Endothelial progenitor cells (EPCs) play a vital role in endothelial repair following vascular injury by maintaining the integrity of endothelium. As EPCs home to endothelial injury sites, they may communicate with exposed vascular smooth muscle cells (VSMCs), which are subjected to cyclic stretch generated by blood flow. In this study, the synergistic effect of cyclic stretch and communication with neighboring VSMCs on EPC function during vascular repair was investigated. Read More

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December 2020

BMP9 and BMP10 Act Directly on Vascular Smooth Muscle Cells for Generation and Maintenance of the Contractile State.

Circulation 2021 Apr 18;143(14):1394-1410. Epub 2020 Dec 18.

Departments of Cardiac Development and Remodeling (L.W., M.R., S.S., F.W., T.B., M.W., A.S., T.B.).

Background: Vascular smooth muscle cells (VSMCs) show a remarkable phenotypic plasticity, allowing acquisition of contractile or synthetic states, but critical information is missing about the physiologic signals, promoting formation, and maintenance of contractile VSMCs in vivo. BMP9 and BMP10 (bone morphogenetic protein) are known to regulate endothelial quiescence after secretion from the liver and right atrium, whereas a direct role in the regulation of VSMCs was not investigated. We studied the role of BMP9 and BMP10 for controlling formation of contractile VSMCs. Read More

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