Abstract
The phenotypic transformation and dysfunctions of vascular smooth muscle cells (SMCs) such as abnormality proliferation and apoptosis are key pathological basis of atherosclerosis. The recent study aimed to detect the role of miR-29b in phenotypic transformation of SMCs. In this study, we investigated the expression level of miR-29b and MMP-2 in acute coronary syndrome (ACS) patients, verified whether MMP-2 is the target gene of miR-29b by luciferase reporter gene system, and explored the role of miR-29b in the viability and apoptosis of SMCs. We found that the plasma level of miR-29b was significantly downregulated to 56% of controls (p < 0.01). The plasma level of MMP-2 in health controls was 34.9 ± 6.9 ng/mL, and that it significantly increased to 46.2 ± 13.2 ng/mL in ACS patients. MMP-2 is a target gene of miR-29b. The overexpression of miR-29b significantly downregulated the expression of MMP-2 mRNA and protein. miR-29b mimics inhibited the cell viability of SMCs, and cell apoptosis was significantly enhanced compared with the NC group, especially in the early stage. In the presence of MMP-2 inhibitor SB-3CT, the cell viability and apoptosis of SMC cells were significantly reduced and enhanced, respectively, while the miR-29b -inhibited cell viability and -induced cell apoptosis were not significantly changed. Taken together, miR-29b was downregulated in ACS patients. MiR-29 mimics inhibits cell viability and promotes cell apoptosis via directly targeting on MMP-2, which could be a potentially promising therapy target for cardiovascular diseases.