Journal of Cellular Biochemistry

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

Authors

  • Myung-Hyun Kim,

    1. Cardiology Division, Heart Center, Gangnam Severance Hospital, Yonsei University College of Medicine, Republic of Korea
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  • Onju Ham,

    1. Cardiovascular Research Institute, Yonsei University College of Medicine, Republic of Korea
    2. Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Republic of Korea
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  • Se-Yeon Lee,

    1. Cardiovascular Research Institute, Yonsei University College of Medicine, Republic of Korea
    2. Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Republic of Korea
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  • Eunmi Choi,

    1. Severance Biomedical Science Institute, Yonsei University College of Medicine, Republic of Korea
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  • Chang Youn Lee,

    1. Department of Integrated Omics for Biomedical Sciences, Graduate School, Yonsei University, Republic of Korea
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  • Jun-Hee Park,

    1. Department of Integrated Omics for Biomedical Sciences, Graduate School, Yonsei University, Republic of Korea
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  • Jiyun Lee,

    1. Cardiovascular Research Institute, Yonsei University College of Medicine, Republic of Korea
    2. Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Republic of Korea
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  • Hyang-Hee Seo,

    1. Cardiovascular Research Institute, Yonsei University College of Medicine, Republic of Korea
    2. Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Republic of Korea
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  • Minji Seung,

    1. Cardiovascular Research Institute, Yonsei University College of Medicine, Republic of Korea
    2. Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Republic of Korea
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  • Eunhyun Choi,

    1. Severance Integrative Research Institute for Cerebral & Cardiovascular Disease, Yonsei University Health System, Republic of Korea
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  • Pil-Ki Min,

    1. Cardiology Division, Heart Center, Gangnam Severance Hospital, Yonsei University College of Medicine, Republic of Korea
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  • Ki-Chul Hwang

    Corresponding author
    1. Cardiovascular Research Institute, Yonsei University College of Medicine, Republic of Korea
    2. Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Republic of Korea
    3. Severance Biomedical Science Institute, Yonsei University College of Medicine, Republic of Korea
    • Correspondence to: Ki-Chul Hwang, Severance Biomedical Science Institute, Cardiovascular Research Institute, Yonsei University College of Medicine, 250 Seongsanno, Seodamun-gu, Seoul 120-752, Republic of Korea. E-mail: kchwang@yuhs.ac

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  • The authors declared that they have no conflicts of interest.

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. J. Cell. Biochem. 115: 1752–1761, 2014. © 2014 Wiley Periodicals, Inc.

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