Myocardin inhibited the gap protein connexin 43 via promoted miR-206 to regulate vascular smooth muscle cell phenotypic switch.
Myocardin is regarded as a key mediator for the change of smooth muscle phenotype. The gap junction protein connexin 43 (Cx43) has been shown to be involved in vascular smooth muscle cells (VSMCs) proliferation and the development of atherosclerosis. However, the role of myocardin on gap junction of cell communication and the relation between myocardin and Cx43 in VSMC phenotypic switch has not been investigated. The goal of the present study is to investigate the molecular mechanism by which myocardin affects Cx43-regulated VSMC proliferation. Data presented in this study demonstrated that inhibition of the Cx43 activation process impaired VSMC proliferation. On the other hand, overexpression miR-206 inhibited VSMC proliferation. In additon, miR-206 silences the expression of Cx43 via targeting Cx43 3' Untranslated Regions. Importantly, myocardin can significantly promote the expression of miR-206. Cx43 regulates VSMCs' proliferation and metastasis through miR-206, which could be promoted by myocardin and used as a marker for diagnosis and a target for therapeutic intervention. Thus myocardin affected the gap junction by inhibited Cx43 and myocardin-miR-206-Cx43 formed a loop to regulate VSMC phenotypic switch.
Institute of Biology and Medicine, Wuhan University of Science and Technology, 430000, PR China.
Hui
H
Li
Institute of Biology and Medicine, Wuhan University of Science and Technology, 430000, PR China.
Yuan
Y
Xiang
Institute of Biology and Medicine, Wuhan University of Science and Technology, 430000, PR China.
Li-Juan
LJ
Fan
Institute of Biology and Medicine, Wuhan University of Science and Technology, 430000, PR China.
Xiao-Yu
XY
Zhang
Institute of Biology and Medicine, Wuhan University of Science and Technology, 430000, PR China.
Jia-Peng
JP
Li
Institute of Biology and Medicine, Wuhan University of Science and Technology, 430000, PR China.
Cheng-Xi
CX
Yu
Institute of Biology and Medicine, Wuhan University of Science and Technology, 430000, PR China.
Le-Yuan
LY
Bao
Institute of Biology and Medicine, Wuhan University of Science and Technology, 430000, PR China.
Dong-Sun
DS
Cao
Institute of Biology and Medicine, Wuhan University of Science and Technology, 430000, PR China.
Wei-Bing
WB
Xing
Institute of Biology and Medicine, Wuhan University of Science and Technology, 430000, PR China; Key Laboratory of Industrial Fermentation Microbiology, Ministry of Education and Tianjin, College of Biotechnology, Tianjin University of Science and Technology, 300457, PR China. Electronic address: xinghualiao@hotmail.com.
Xing-Hua
XH
Liao
Institute of Biology and Medicine, Wuhan University of Science and Technology, 430000, PR China; Key Laboratory of Industrial Fermentation Microbiology, Ministry of Education and Tianjin, College of Biotechnology, Tianjin University of Science and Technology, 300457, PR China. Electronic address: zhangtongcun@wust.edu.cn.
Tong-Cun
TC
Zhang
D020413:3' Untranslated Regions; D002454:Cell Differentiation; D002460:Cell Line; D049109:Cell Proliferation; D018031:Connexin 43 / Q000235:genetics* / Q000378:metabolism; D006801:Humans; D035683:MicroRNAs / Q000235:genetics*; D009131:Muscle, Smooth, Vascular / Q000166:cytology* / Q000378:metabolism; D009687:Nuclear Proteins / Q000378:metabolism*; D010641:Phenotype; D015534:Trans-Activators / Q000378:metabolism*; D000099251:Myocardin
D020413:3' Untranslated Regions; D018031:Connexin 43; D035683:MicroRNAs; D009687:Nuclear Proteins; D015534:Trans-Activators; D000099251:Myocardin; C500216:GJA1 protein, human; C546087:MIRN206 microRNA, human
Connexin 43; Myocardin; Vascular smooth muscle cell phenotypic switch; miR-206