Lijun Liu1, Ziping Cheng2, Jie Yang2. 1. Department of Cardiovascular Medicine, Huainan First People's Hospital, Huainan, Anhui, 232007, PR China. Electronic address: lijun_liu23@163.com. 2. Department of Cardiovascular Medicine, The First Affiliated Hospital of Anui Medical University, Hefei, Anhui, 230022, PR China.
Abstract
BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSION: Our findings suggest that miR-23 plays a crucial role in controlling VSMCs proliferation and apoptosis by targeting BCL2L11.
BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSION: Our findings suggest that miR-23 plays a crucial role in controlling VSMCs proliferation and apoptosis by targeting BCL2L11.
Authors: Sylwia Iwańczyk; Tomasz Lehmann; Artur Cieślewicz; Artur Radziemski; Katarzyna Malesza; Michał Wrotyński; Paweł P Jagodziński; Marek Grygier; Maciej Lesiak; Aleksander Araszkiewicz Journal: Exp Ther Med Date: 2022-04-21 Impact factor: 2.751
Authors: Václava Černá; Pavel Ostašov; Pavel Pitule; Jiří Moláček; Vladislav Třeška; Martin Pešta Journal: Cardiol Res Pract Date: 2019-11-29 Impact factor: 1.866