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MicroRNA-365 Inhibits the Proliferation of Vascular Smooth Muscle Cells by Targeting Cyclin D1

Authors
 Myung-Hyun Kim  ;  Onju Ham  ;  Se-Yeon Lee  ;  Eunmi Choi  ;  Chang Youn Lee  ;  Jun-Hee Park  ;  Jiyun Lee  ;  Hyang-Hee Seo  ;  Minji Seung  ;  Eunhyun Choi  ;  Pil-Ki Min  ;  Ki-Chul Hwang 
Citation
 Journal of Cellular Biochemistry, Vol.115(10) : 1752-1761, 2014 
Journal Title
 Journal of Cellular Biochemistry 
ISSN
 0730-2312 
Issue Date
2014
MeSH
Angiotensin II/pharmacology ; Animals ; Atherosclerosis/pathology* ; Carotid Arteries/metabolism ; Carotid Artery Injuries/metabolism ; Cell Division/genetics ; Cell Movement/genetics ; Cell Proliferation/genetics ; Cells, Cultured ; Cyclin D1/biosynthesis* ; Down-Regulation ; MicroRNAs/biosynthesis ; MicroRNAs/genetics* ; Muscle, Smooth, Vascular/cytology ; Muscle, Smooth, Vascular/growth & development* ; Neointima/genetics* ; Proliferating Cell Nuclear Antigen/biosynthesis ; Protein Binding ; Proto-Oncogene Proteins c-sis/pharmacology ; RNA-Binding Proteins ; Rats ; S Phase Cell Cycle Checkpoints/genetics
Keywords
CELL CYCLE ; CYCLIN D1 ; MIR-365 ; PROLIFERATION ; VASCULAR SMOOTH MUSCLE CELLS
Abstract
Abnormal proliferation of vascular smooth muscle cells (VSMCs) is a common feature of disease progression in atherosclerosis. Cell proliferation is regulated by cell cycle regulatory proteins. MicroRNAs (miR) have been reported to act as important gene regulators and play essential roles in the proliferation and migration of VSMCs in a cardiovascular disease. However, the roles and mechanisms of miRs in VSMCs and neointimal formation are far from being fully understood. In this study, cell cycle-specific cyclin D1 was found to be a potential target of miR-365 by direct binding. Through an in vitro experiment, we showed that exogenous miR-365 overexpression reduced VSMC proliferation and proliferating cell nuclear antigen (PCNA) expression, while miR-365 was observed to block G1/S transition in platelet-derived growth factor-bb (PDGF-bb)-induced VSMCs. In addition, the proliferation of VSMCs by various stimuli, including PDGF-bb, angiotensin II (Ang II), and serum, led to the downregulation of miR-365 expression levels. The expression of miR-365 was confirmed in balloon-injured carotid arteries. Taken together, our results suggest an anti-proliferative role for miR-365 in VSMC proliferation, at least partly via modulating the expression of cyclin D1. Therefore, miR-365 may influence neointimal formation in atherosclerosis patients.
Full Text
http://onlinelibrary.wiley.com/doi/10.1002/jcb.24841/abstract
DOI
10.1002/jcb.24841
Appears in Collections:
5. Research Institutes (연구소) > Yonsei Integrative Research Institute for Cerebral & Cardiovascular Disease (뇌심혈관질환융합연구사업단) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers
Yonsei Authors
Kim, Myung Hyun(김명현)
Min, Pil Ki(민필기) ORCID logo https://orcid.org/0000-0001-7033-7651
Park, Jun-Hee(박준희)
Seo, Hyang Hee(서향희)
Lee, Se Yeon(이세연)
Lee, Chang Yeon(이창연)
Choi, Eun Mi(최은미)
Choi, Eun Hyun(최은현)
Ham, On Ju(함온주)
Hwang, Ki Chul(황기철)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/99826
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