Liu Lijun, Cheng Ziping, Yang Jie
Department of Cardiovascular Medicine, Huainan First People's Hospital, Huainan, Anhui, 232007, PR China.
Department of Cardiovascular Medicine, The First Affiliated Hospital of Anui Medical University, Hefei, Anhui, 230022, PR China.
Pathol Res Pract. 2018 Nov;214(11):1873-1878. doi: 10.1016/j.prp.2018.09.004. Epub 2018 Sep 13.
Aberrant proliferation and migration of vascular smooth muscle cells (VSMCs) play an important role in the pathogenesis of cardiovascular diseases including coronary heart disease (CHD). MicroRNAs has reported play critical roles in VSMCs function. The present study was to investigate the effects of microRNA‑23 (miR-23) on VSMCs and uncover its potential mechanism.
Cell viability was detected by CCK-8 assay. Cell apoptosis was measured by flow cytometry. Dual luciferase reporter assay was conducted to verify whether BCL2L11 is a target gene of miR-23. The protein levels of BCL2L11 and caspase-3 were detect by quantitative real time PCR and western blot.
Our results showed that the expression of miR-23 was upregulated in peripheral blood of CHD patients compared with controls. Overexpression of miR-23 promoted VSMCs proliferation and inhibited VSMCs apoptosis. Downregulation of miR-23 suppressed VSMCs proliferation and promoted VSMCs apoptosis. In addition, we identified BCL2L11 was a direct gene of miR-23. Overexpression of miR-23 decreased the levels of BCL2L11 and caspase-3, and downregulate of miR-23 increased the levels of BCL2L11and caspase-3 in VSMCs.
Our findings suggest that miR-23 plays a crucial role in controlling VSMCs proliferation and apoptosis by targeting BCL2L11.
血管平滑肌细胞(VSMC)的异常增殖和迁移在包括冠心病(CHD)在内的心血管疾病发病机制中起重要作用。据报道,微小RNA在VSMC功能中起关键作用。本研究旨在探讨微小RNA-23(miR-23)对VSMC的影响并揭示其潜在机制。
采用CCK-8法检测细胞活力。通过流式细胞术检测细胞凋亡。进行双荧光素酶报告基因检测以验证BCL2L11是否为miR-23的靶基因。通过定量实时PCR和蛋白质印迹法检测BCL2L11和半胱天冬酶-3的蛋白水平。
我们的结果表明,与对照组相比,CHD患者外周血中miR-23的表达上调。miR-23的过表达促进VSMC增殖并抑制VSMC凋亡。miR-23的下调抑制VSMC增殖并促进VSMC凋亡。此外,我们确定BCL2L11是miR-23的直接靶基因。miR-23的过表达降低了VSMC中BCL2L11和半胱天冬酶-3的水平,而miR-23的下调增加了BCL2L11和半胱天冬酶-3的水平。
我们的研究结果表明,miR-23通过靶向BCL2L11在控制VSMC增殖和凋亡中起关键作用。