Zhenduanxue lilun yu shijian (Feb 2021)

Preliminary study on the role of miR-16 in progression of coronary atherosclerosis and possible molecular mechanism

  • ZHA Qing, YU Chenxi, LIU Ya, YANG Ling, YE Jiawen, LIU Yan

DOI
https://doi.org/10.16150/j.1671-2870.2021.01.013
Journal volume & issue
Vol. 20, no. 01
pp. 82 – 87

Abstract

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Objective: To explore the role of microRNA (miRNA, miR) -16 in the development of coronary atheromatous plaques and to study possible mechanism involved in the process. Methods: Coronary artery tissues were obtained from 16 patients undergoing coronary artery bypass grafting,and the coronary artery plaques were divided into fibrous plaques and atheromatous plaques based on pathological examination. The expression level of miR-16 in coronary fibrous plaques and atheromatous plaques was detected by miRNAs array. The in vitro model of oxidized low density lipoprotein (oxLDL)-induced foam cells from macrophages was established, the transformation as well as apoptosis of foam cells were detected by TUNEL assay, cell counting and Western blotting. The release of inflammatory cytokines [interleukin (IL)-6, IL-8, monocyte chemoattractant protein (MCP)-1 and matrix metalloproteinase (MMP)-9] in the culture supernatant of form cell was tested by enzyme-linked immunosorbent assay(ELISA), and expression of miR-16 was tested by miRNAs array. Finally, miR-16 was transfected into macrophages and the apoptosis of foam cell as well as the release of inflammatory factors were detected. Results: Compared with fibrous plaques of coronary artery, the expression of miR-16 in coronary atheromatous plaques detected by miRNAs assay increased by 1.75 folds. In vitro model of oxLDL-induced foam cells showed that oxLDL might promote the transfer of macrophages into foam cells and induce foam cells apoptosis and stimulate the release of inflammatory factors (such as IL-6, IL-8, MCP-1 and MMP-9). Macrophages transfected with miR-16 could further induce the apoptosis of foam cells and secretion of inflammatory factors. Conclusions: oxLDL could induce the apoptosis of foam cells, release of inflammatory factors and up-regulate miR-16 expression, and the high expression of miR-16 could further enhance foam cell apoptosis and inflammatory response, further promote the progression of atherosclerosis. miR-16 might serve as a potential target for inhibiting artherosclerosis.

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