The anti-inflammatory effect of miR-16 through targeting C- reactive protein is regulated by HuR in vascular smooth muscle cells.

Atherosclerosis (AS) is the main pathological basis of coronary heart disease (CHD). Vascular smooth muscle cells (VMSCs) proliferation, migration and inflammatory response are the cytopathologic basis of AS. MiR-16 has been suggested to be closely associated with cell proliferation and inflammation. The regulatory role of the RNA binding protein HuR on miR-16 has been reported in colon cancer. However, the underlying roles of miR-16 on VMSCs and the regulatory function of HuR on miR-16 in VMSCs remain unknown. In this study, we found that the expression of miR-16 reduced and the expression of C-reactive protein and HuR increased when contractile VSMCs transformed into synthetic VMSCs. Furthermore, miR-16 impeded cell proliferation and inflammation via targeting CRP in VMSCs. HuR down-regulated miR-16 expression and impeded its influence on VMSCs. This study might provide an opportunity to develop a new effective target for the treatment of CHD.

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