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- Title
MicroRNA-204 regulates vascular smooth muscle cell calcification in vitro and in vivo.
- Authors
Cui, Rong-Rong; Li, Shi-Jun; Liu, Ling-Juan; Yi, Lu; Liang, Qiu-Hua; Zhu, Xiao; Liu, Guan-Ying; Liu, Yuan; Wu, Shan-Shan; Liao, Xiao-Bo; Yuan, Ling-Qing; Mao, Ding-An; Liao, Er-Yuan
- Abstract
Aims Medial artery calcification is a common macroangiopathy that initiates from a cell-regulated process similar to osteogenesis. Although the mechanisms governing this process remain unclear, epigenomic regulation by specific microRNAs might play a role in vascular smooth muscle cell (VSMC) calcification. In this study, we aimed to investigate whether miR-204 participates in the regulation of VSMC calcification. Methods and results We found that miR-204 was suppressed in mouse aortic VSMCs during β-glycerophosphate-induced calcification, whereas Runx2 protein levels were elevated. Overexpression of miR-204 by transfection of miR-204 mimics decreased Runx2 protein levels and alleviated β-glycerophosphate-induced osteoblastic differentiation of VSMCs, whereas miR-204 inhibition by transfection of miR-204 inhibitors significantly elevated Runx2 protein levels and enhanced osteoblastic differentiation of VSMCs, suggesting the role of miR-204 as an endogenous attenuator of Runx2 in VSMC calcification. Luciferase reporter assays revealed Runx2 as the direct target of miR-204 by overexpression of miR-204 on the wild-type or mutant 3′-UTR sequences of Runx2 in VSMCs. In vivo overexpression of miR-204 by injection of miR-204 agomirs in Kunming mice attenuated vitamin D3-induced medial artery calcification. Conclusion Our study has shown that down-regulation of miR-204 may contribute to β-glycerophosphate-induced VSMC calcification through regulating Runx2. miR-204 represents an important new regulator of VSMC calcification and a potential therapeutic target in medial artery calcification.
- Subjects
MICRORNA; VASCULAR smooth muscle; MUSCLE cells; CALCIFICATION; BONE growth; GENE transfection; BIOLOGICAL assay
- Publication
Cardiovascular Research, 2012, Vol 96, Issue 2, p320
- ISSN
0008-6363
- Publication type
Article
- DOI
10.1093/cvr/cvs258