MicroRNA-24-3p inhibition prevents cell growth of vascular smooth muscle cells by targeting Bcl-2-like protein 11.

Numerous reports have shown that dysfunction of vascular smooth muscle cells (VSMCs) serves a critical function in the development of cardiovascular disease, including coronary heart disease (CHD). microRNAs (miRNAs/miRs) have been reported to play important roles in regulating the function of VSMCs. The present study aimed to determine the role of miR-24-3p in VSMCs and to uncover the underlying mechanism. The expression of miR-24-3p in the peripheral blood samples of CHD patients was measured by reverse transcription-quantitative (RT-q)PCR. It was found that the level of miR-24-3p in the peripheral blood of patients with CHD was significantly upregulated compared with that in healthy controls. A dual luciferase reporter assay was performed to determine whether Bcl-2-like protein 11 (Bcl-2L11) was a target gene of miR-24-3p, and it was identified that Bcl-2L11 was a direct target of miR-24-3p. The mRNA level and protein expression of Bcl-2L11 in the peripheral blood of patients with CHD were measured by RT-qPCR and western blotting, respectively. The findings suggested that Bcl-2L11 was downregulated in the peripheral blood of patients with CHD. In addition, it was found that downregulation of miR-24-3p suppressed VSMC proliferation and promoted VSMC apoptosis, while the effects of the miR-24-3p inhibitor on cell viability and apoptosis were reversed by Bcl-2L11-small interfering (si)RNA. Additionally, downregulation of miR-24-3p increased the levels of Bcl-2L11, caspase-3 and Bax, and decreased Bcl-2 expression in VSMCs; these changes were abolished by Bcl-2L11-siRNA. In conclusion, the aforementioned results indicated that miR-24-3p was an important regulator in VSMC proliferation and apoptosis by targeting Bcl-2L11, which suggested that miR-24-3p might be a potential therapeutic target for the treatment of CHD.