Qu Yunfei, Zhang Ning
Department of Cardiac Vascular Surgery, Chongqing Three Gorges Central Hospital, Chongqing 404000, P.R. China.
Department of General Medicine, Chongqing Three Gorges Central Hospital, Chongqing 404000, P.R. China.
Exp Ther Med. 2018 Nov;16(5):4239-4245. doi: 10.3892/etm.2018.6720. Epub 2018 Sep 11.
Abnormal proliferation and migration of vascular smooth muscle cells serves a crucial role in the development of atherosclerosis. Previous studies have suggested that some microRNAs (miRs) are involved in this process; however, the associated underlying molecular mechanism is unclear. In present study, human coronary artery smooth muscle cells (HCASMCs) were used to explore the function of miR-365b-3p in the coronary atherosclerosis. It was indicated that platelet-derived growth factor-BB (PDGF-BB) treatment inhibited miR-365b-3p expression and upregulated the expression of a disintegrin and metalloproteinase with thrombospondin motifs 1 (ADAMTS1) in HCASMCs. Subsequently, miR-365b-3p mimic was transfected in HCASMCs to explore the function of this miR. The results of reverse transcription-quantitative polymerase chain reaction and western blot analysis indicated that overexpression of miR-365b-3p significantly downregulated ADAMTS1 expression. Functional assay results revealed that overexpression of miR-365b-3p significantly attenuated PDGF-BB-induced proliferation and migration of HCASMCs. Furthermore, the dual-luciferase reporter assay results confirmed that ADAMTS1 is a direct target gene of miR-365b-3p. This discovery proposed a novel channel of communication between ADAMTS1 and HCASMCs, and suggests a potential therapeutic approach for coronary atherosclerosis.
血管平滑肌细胞的异常增殖和迁移在动脉粥样硬化的发展中起着关键作用。先前的研究表明，一些微小RNA（miRs）参与了这一过程；然而，相关的潜在分子机制尚不清楚。在本研究中，使用人冠状动脉平滑肌细胞（HCASMCs）来探讨miR-365b-3p在冠状动脉粥样硬化中的作用。结果表明，血小板衍生生长因子-BB（PDGF-BB）处理抑制了HCASMCs中miR-365b-3p的表达，并上调了含血小板反应蛋白基序的解聚素和金属蛋白酶1（ADAMTS1）的表达。随后，将miR-365b-3p模拟物转染到HCASMCs中以探究该miR的功能。逆转录-定量聚合酶链反应和蛋白质印迹分析结果表明，miR-365b-3p的过表达显著下调了ADAMTS1的表达。功能测定结果显示，miR-365b-3p的过表达显著减弱了PDGF-BB诱导的HCASMCs增殖和迁移。此外，双荧光素酶报告基因测定结果证实ADAMTS1是miR-365b-3p的直接靶基因。这一发现提出了ADAMTS1与HCASMCs之间一种新的通讯途径，并提示了一种针对冠状动脉粥样硬化的潜在治疗方法。
