| First Author | Cui RR | Year | 2012 |
| Journal | Cardiovasc Res | Volume | 96 |
| Issue | 2 | Pages | 320-9 |
| PubMed ID | 22871591 | Mgi Jnum | J:202650 |
| Mgi Id | MGI:5520154 | Doi | 10.1093/cvr/cvs258 |
| Citation | Cui RR, et al. (2012) MicroRNA-204 regulates vascular smooth muscle cell calcification in vitro and in vivo. Cardiovasc Res 96(2):320-9 |
| abstractText | 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 beta-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 beta-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 beta-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. |
