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vsmc differentiation

Y Xiao, Y Y DU, C Gao, W Kong
OBJECTIVE: To study the change of microRNA during the early stage of high phosphorus induced vascular smooth muscle cell (VSMC) calcification and its related mechanism. METHODS: The in vitro calcification model was created through stimulating VSMC cell line A7r5 with high Pi (2.6 mmol/L) for 7 d. The calcification was validated through ocresolphthalein complexone colorimetry to detect the cellular calcium content, real-time PCR to measure the calcification-related gene expression and alizarin red staining to observe the formation of calcium nodules...
October 18, 2016: Beijing da Xue Xue Bao. Yi Xue Ban, Journal of Peking University. Health Sciences
Xin Guo, Dai Li, Min Chen, Lei Chen, Bikui Zhang, Tian Wu, Ren Guo
Recent studies have demonstrated functions of miR-145 in vascular smooth muscle cells (VSMCs) phenotypes and vascular diseases. In this study, we aim to determine whether CD40 is involved in miR-145 mediated switch of VSMC phenotypes. In cultured VSMCs, the effects of miR-145 and CD40 on TNF-α, TGF-β, and Homocysteine (Hcy) induced cell proliferation were evaluated by over-expression of miR-145 or by siRNA-mediated knockdown of CD40. We also used ultrasound imaging to explore the effect of miR-145 on carotid artery intima-media thickness (CIMT) in atherosclerotic cerebral infarction (ACI) patients...
October 12, 2016: Scientific Reports
Daliang Yan, Xiaojuan Liu, Lu Hua, Kunpeng Wu, Xilin Sha, Jianhua Zhao, Chen Yang, Chao Zhang, Jiahai Shi, Xiang Wu
Cardiac allograft vasculopathy (CAV) was the leading cause of late death in heart transplantation recipients. Matrix metalloproteinase-14 (MMP-14), as a member of the MMPs family, has been reported to play a vital role in coronary vascular lesions of allotransplanted hearts. However, concrete mechanism is still unclear. Herein, we showed that the expression of MMP-14 was different between isografts and allografts. Interestingly, we found MMP-14 could interact with CD44 in allografts. Cluster of differentiation 44 (CD44), as a cell adhesion receptor and is involved in cell migration, caused our interest in MMP-14/CD44 complex in allografts...
September 25, 2016: Pathology, Research and Practice
Chien-Hung Huang, Jin-Shuei Ciou, Shun-Tsung Chen, Victor C Kok, Yi Chung, Jeffrey J P Tsai, Nilubon Kurubanjerdjit, Chi-Ying F Huang, Ka-Lok Ng
BACKGROUND: Abnormal proliferation of vascular smooth muscle cells (VSMC) is a major cause of cardiovascular diseases (CVDs). Many studies suggest that vascular injury triggers VSMC dedifferentiation, which results in VSMC changes from a contractile to a synthetic phenotype; however, the underlying molecular mechanisms are still unclear. METHODS: In this study, we examined how VSMC responds under mechanical stress by using time-course microarray data. A three-phase study was proposed to investigate the stress-induced differentially expressed genes (DEGs) in VSMC...
2016: PeerJ
Joel Chappell, Jennifer L Harman, Vagheesh M Narasimhan, Haixiang Yu, Kirsty Foote, Benjamin D Simons, Martin R Bennett, Helle F Jorgensen
RATIONALE: Vascular smooth muscle cell (VSMC) accumulation is a hallmark of atherosclerosis and vascular injury. However, fundamental aspects of proliferation and the phenotypic changes within individual VSMCs, which underlie vascular disease remain unresolved. In particular, it is not known if all VSMCs proliferate and display plasticity, or whether individual cells can switch to multiple phenotypes. OBJECTIVE: To assess whether proliferation and plasticity in disease is a general characteristic of VSMCs or a feature of a subset of cells...
September 28, 2016: Circulation Research
Min Jin, Yutao Wu, Yanwei Wang, Danqing Yu, Mei Yang, Feng Yang, Chun Feng, Ting Chen
MicroRNA-29a (miR-29a) has been extensively studied in tumor biology and fibrotic diseases, but little is known about its functional roles in vascular smooth muscle cell (VSMC) differentiation from embryonic stem cells (ESCs). Using well-established VSMC differentiation models, we have observed that miR-29a induces VSMC differentiation from mouse ESCs by negatively regulating YY1, a transcription factor that inhibits muscle cell differentiation and muscle-specific gene expression. Moreover, gene expression levels of three VSMC specific transcriptional factors were up-regulated by miR-29a over-expression, but down-regulated by miR-29a inhibition or YY1 over-expression...
August 2, 2016: Stem Cell Research
Lunchang Wang, Ping Qiu, Jiao Jiao, Hiroyuki Hirai, Wei Xiong, Jifeng Zhang, Tianqing Zhu, Peter X Ma, Y Eugene Chen, Bo Yang
Vascular smooth muscle cells (VSMCs) derived from cardiovascular progenitor cell (CVPC) lineage populate the tunica media of the aortic root. Understanding differentiation of VSMCs from CVPC will further our understanding of the molecular mechanisms contributing to aortic root aneurysms, and thus, facilitate the development of novel therapeutic agents to prevent this devastating complication. It is established that the yes-associated protein (YAP) and Hippo pathway is important for VSMC proliferation and phenotype switch...
August 29, 2016: Stem Cells
Sukrutha Chettimada, Sachindra Raj Joshi, Vidhi Dhagia, Alessandro Aiezza, Thomas M Lincoln, Rakhee Gupte, Joseph M Miano, Sachin A Gupte
Homeostatic control of vascular smooth muscle cell (VSMC) differentiation is critical for contractile activity and regulation of blood flow. Recently, we reported that precontracted blood vessels are relaxed and the phenotype of VSMC is regulated from a synthetic to contractile state by glucose-6-phosphate dehydrogenase (G6PD) inhibition. In the current study, we investigated whether the increase in the expression of VSMC contractile proteins by inhibition and knockdown of G6PD is mediated through a protein kinase G (PKG)-dependent pathway and whether it regulates blood pressure...
October 1, 2016: American Journal of Physiology. Heart and Circulatory Physiology
Menglin Hou, Yan Song, Zhenlin Li, Chufan Luo, Jing-Song Ou, Huimin Yu, Jianyun Yan, Lihe Lu
Vascular calcification has been considered as a biological process resembling bone formation involving osteogenic differentiation. It is a major risk factor for cardiovascular morbidity and mortality. Previous studies have shown the protective effects of curcumin on cardiovascular diseases. However, whether curcumin has effects on osteogenic differentiation and calcification of vascular smooth muscle cells (VSMCs) has not been reported. In the present study, we used an in vitro model of VSMC calcification to investigate the role of curcumin in the progression of rat VSMC calcification...
September 2016: Molecular and Cellular Biochemistry
Yue Liu, Fang Lin, Yu Fu, Wenjia Chen, Wenxiu Liu, Jinyu Chi, Xiaohui Zhang, Xinhua Yin
Accumulating evidence has indicated that vascular smooth muscular cells (VSMCs) play an important role in the development of vascular calcification (VC). Cortistatin (CST), a novel bio-active peptide, has been shown to exert multiple protective effects on the cardiovascular system. However, the role and possible mechanism of CST in VC remain unclear. Therefore, we used β-glycerophosphoric acid (β-GP) to induce calcification in rat and human VSMCs to determine the effects of CST on osteoblastic differentiation and VSMC mineralization in vitro...
November 2016: Amino Acids
Sophie Mokas, Richard Larivière, Laurent Lamalice, Stéphane Gobeil, David N Cornfield, Mohsen Agharazii, Darren E Richard
Medial vascular calcification is a common complication of chronic kidney disease (CKD). Although elevated inorganic phosphate stimulates vascular smooth muscle cell (VSMC) osteogenic transdifferentiation and calcification, the mechanisms involved in their calcification during CKD are not fully defined. Because hypoxic gene activation is linked to CKD and stimulates bone cell osteogenic differentiation, we used in vivo and in vitro rodent models to define the role of hypoxic signaling during elevated inorganic phosphate-induced VSMC calcification...
September 2016: Kidney International
Sun-Hwa Song, Kyungjong Kim, Eun-Kyung Jo, Young-Wook Kim, Jin-Sook Kwon, Sun Sik Bae, Jong-Hyuk Sung, Sang Gyu Park, Jee Taek Kim, Wonhee Suh
OBJECTIVE: Vascular smooth muscle cells (VSMCs) modulate their phenotype between synthetic and contractile states in response to environmental changes; this modulation plays a crucial role in the pathogenesis of restenosis and atherosclerosis. Here, we identified fibroblast growth factor 12 (FGF12) as a novel key regulator of the VSMC phenotype switch. APPROACH AND RESULTS: Using murine models and human specimens, we found that FGF12 was highly expressed in contractile VSMCs of normal vessel walls but was downregulated in synthetic VSMCs from injured and atherosclerotic vessels...
September 2016: Arteriosclerosis, Thrombosis, and Vascular Biology
Alexis Régent, Kim Heang Ly, Sébastien Lofek, Guilhem Clary, Mathieu Tamby, Nicolas Tamas, Christian Federici, Cédric Broussard, Philippe Chafey, Emmanuelle Liaudet-Coopman, Marc Humbert, Frédéric Perros, Luc Mouthon
Vascular smooth muscle cells (VSMCs) are highly specialized cells that regulate vascular tone and participate in vessel remodeling in physiological and pathological conditions. It is unclear why certain vascular pathologies involve one type of vessel and spare others. Our objective was to compare the proteomes of normal human VSMC from aorta (human aortic smooth muscle cells, HAoSMC), umbilical artery (human umbilical artery smooth muscle cells, HUASMC), pulmonary artery (HPASMC), or pulmonary artery VSMC from patients with pulmonary arterial hypertension (PAH-SMC)...
October 2016: Proteomics
Jinjing Zhao, Wei Zhang, Mingyan Lin, Wen Wu, Pengtao Jiang, Emiley Tou, Min Xue, Angelene Richards, David Jourd'heuil, Arif Asif, Deyou Zheng, Harold A Singer, Joseph M Miano, Xiaochun Long
OBJECTIVE: Long noncoding RNAs (lncRNA) represent a growing class of noncoding genes with diverse cellular functions. We previously reported on SENCR, an lncRNA that seems to support the vascular smooth muscle cell (VSMC) contractile phenotype. However, information about the VSMC-specific lncRNAs regulated by myocardin (MYOCD)/serum response factor, the master switch for VSMC differentiation, is unknown. APPROACH AND RESULTS: To define novel lncRNAs with functions related to VSMC differentiation, we performed RNA sequencing in human coronary artery SMCs that overexpress MYOCD...
October 2016: Arteriosclerosis, Thrombosis, and Vascular Biology
ChengJian Cao, HuiPing Zhang, Li Zhao, Longxia Zhou, Minghao Zhang, Hua Xu, Xuebo Han, Guizhong Li, Xiaoling Yang, YiDeng Jiang
MicroRNAs (miRNAs) are short non-coding RNA and play crucial roles in a wide array of biological processes, including cell proliferation, differentiation and apoptosis. Our previous studies found that homocysteine(Hcy) can stimulate the proliferation of vascular smooth muscle cells (VSMCs), however, the underlying mechanisms were not fully elucidated. Here, we found proliferation of VSMCs induced by Hcy was of correspondence to the miR-125b expression reduced both in vitro and in the ApoE knockout mice, the hypermethylation of p53, its decreased expression, and DNA (cytosine-5)-methyltransferase 3b (DNMT3b) up-regulated...
September 10, 2016: Experimental Cell Research
E Misárková, M Behuliak, M Bencze, J Zicha
Vascular smooth muscle cells (VSMC) display considerable phenotype plasticity which can be studied in vivo on vascular remodeling which occurs during acute or chronic vascular injury. In differentiated cells, which represent contractile phenotype, there are characteristic rapid transient changes of intracellular Ca(2+) concentration ([Ca(2+)]i), while the resting cytosolic [Ca(2+)]i concentration is low. It is mainly caused by two components of the Ca(2+) signaling pathways: Ca(2+) entry via L-type voltage-dependent Ca(2+) channels and dynamic involvement of intracellular stores...
June 20, 2016: Physiological Research
Nick D Tsihlis, Monica P Rodriguez, Qun Jiang, Amanda Schwartz, Megan E Flynn, Janet M Vercammen, Melina R Kibbe
BACKGROUND: Diabetic patients display aggressive restenosis after vascular interventions, likely because of proproliferative influences of hyperglycemia and hyperinsulinemia. We have shown that nitric oxide (NO) inhibits neointimal hyperplasia in type 2, but not in type 1, diabetic rats. Here, we examined proteasome activator 28 (PA28) after arterial injury in different diabetic environments, with or without NO. We hypothesize that NO differentially affects PA28 levels based on metabolic environment...
May 15, 2016: Journal of Surgical Research
Lan Sun, Yongyi Bai, Rui Zhao, Tao Sun, Ruihua Cao, Fuyu Wang, Guorong He, Wen Zhang, Ying Chen, Ping Ye, Guanhua Du
OBJECTIVE: Vascular smooth muscle cell (VSMC) phenotype change is a hallmark of vascular remodeling, which contributes to atherosclerotic diseases and can be regulated via microRNA-dependent mechanisms. We recently identified that asymmetrical dimethylarginine positively correlates to vascular remodeling-based diseases. We hypothesized that asymmetrical dimethylarginine induces smooth muscle cell (SMC) phenotypic change via a microRNA-dependent mechanism. APPROACH AND RESULTS: Microarray analysis enabled the identification of downregulation of miR-182-3p in asymmetrical dimethylarginine-treated human aortic artery SMCs...
July 2016: Arteriosclerosis, Thrombosis, and Vascular Biology
Na Li, Lakshman Subrahmanyan, Emily Smith, Xiaoqing Yu, Samir Zaidi, Murim Choi, Shrikant Mane, Carol Nelson-Williams, Mohadesseh Bahjati, Mohammad Kazemi, Mohammad Hashemi, Mohsen Fathzadeh, Anand Narayanan, Likun Tian, Farhad Montazeri, Mitra Mani, Michael L Begleiter, Brian G Coon, Henry T Lynch, Eric N Olson, Hongyu Zhao, Jürgen Ruland, Richard P Lifton, Arya Mani
Nonsyndromic patent ductus arteriosus (PDA) is a common congenital heart defect (CHD) with both inherited and acquired causes, but the disease mechanisms have remained elusive. Using combined genome-wide linkage analysis and whole-exome sequencing (WES), we identified independent mutations in PRDM6, which encodes a nuclear protein that is specific to vascular smooth muscle cells (VSMC), has histone methyl transferase activities, and acts as a transcriptional suppressor of contractile proteins. In vitro assays showed that the mutations cause loss of function either by intracellular redistribution of the protein and/or by alteration of its methyltransferase activities...
June 2, 2016: American Journal of Human Genetics
Beatriz Ferrán, Ingrid Martí-Pàmies, Judith Alonso, Ricardo Rodríguez-Calvo, Silvia Aguiló, Francisco Vidal, Cristina Rodríguez, José Martínez-González
Recent works have highlighted the role of NOR-1 in both smooth and skeletal muscle, and have proposed this nuclear receptor as a nexus that coordinates muscle performance and metabolic capacity. However, no muscle specific genes regulated by NOR-1 have been identified so far. To identify NOR-1 target genes, we over-expressed NOR-1 in human vascular smooth muscle cells (VSMC). These cells subjected to sustained over-expression of supraphysiological levels of NOR-1 experienced marked phenotypic changes and up-regulated the skeletal muscle protein X-linked (SMPX), a protein typically expressed in striated muscle and associated to cell shape...
2016: Scientific Reports
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