Department of Cardiology, Cardio Cerebrovascular Disease Branch of General Hospital of Ningxia Medical University, No. 6 Ning'an East Lane, Jinfeng District, Yinchuan, Ningxia Province, 750004, China.
J Thromb Thrombolysis. 2021 May;51(4):924-932. doi: 10.1007/s11239-020-02314-1. Epub 2020 Nov 5.
Aberrant vascular smooth muscle cell (VSMCs) proliferation involves in the development of atherosclerosis. It reported that Long noncoding BRAF-activated noncoding RNA (BANCR) and miR-34c played opposite roles in the regulation of the proliferation of VSMCs, indicating that there might be a potential interaction between them. This study was to investigate the relationship between BANCR and miR-34c in atherosclerosis. Blood (5 ml) was obtained from 56 patients with atherosclerosis and 56 healthy volunteers after they were fasted overnight, and plasma was extracted from the blood. Human Aortic Smooth Muscle Cells (HASMCs) were used to perform in vitro cell experiments. RT-qPCR was performed to measure the expression of BANCR and miR-34c in plasma and HASMCs. Dual luciferase reporter assay detected the interaction between BANCR and miR-34c. CCK-8 assay was used to assess the effects of BANCR and miR-34c overexpression on the proliferation of HASMCs. Western blotting was used to assess the effects of BANCR and miR-34c overexpression on the protein expression of HMGB1, TNF-ɑ and Bcl-2. In this study, we found that BANCR was upregulated, while miR-34c was downregulated in atherosclerosis. Bioinformatics analysis showed that BANCR and miR-34c could directly interact with each other. Moreover, overexpression of BANCR could decrease the expression of miR-34c in HASMCs, but overexpression of miR-34c could not affect the expression of BANCR. Furthermore, overexpression of BACNR increased miR-34c methylation, and knockdown of endogenous BANCR decreased miR-34c methylation. In addition, overexpression of BANCR reduced the effects of miR-34c on HASMCs proliferation and reversed the effects of miR-34c on HMGB1, TNF-ɑ and Bcl-2 expression. BANCR overexpression could induce HASMCs proliferation by downregulating the miR-34c methylation. Therefore given BANCR upregulation in atherosclerosis, its expression may be considered as a novel and useful biomarker for atherosclerosis prevention and prognosis. However considering the possible effects of other underlying diseases on both BANCR expression and miR-34c in atherosclerosis, further investigation is suggested for future research.
异常的血管平滑肌细胞（VSMCs）增殖涉及动脉粥样硬化的发展。有报道称，长链非编码 BRAF 激活非编码 RNA（BANCR）和 miR-34c 在调节 VSMCs 增殖方面发挥相反的作用，表明它们之间可能存在潜在的相互作用。本研究旨在探讨动脉粥样硬化中 BANCR 和 miR-34c 之间的关系。禁食过夜后，从 56 例动脉粥样硬化患者和 56 名健康志愿者中抽取 5ml 血液，并从血液中提取血浆。使用人主动脉平滑肌细胞（HASMCs）进行体外细胞实验。采用 RT-qPCR 检测血浆和 HASMCs 中 BANCR 和 miR-34c 的表达。双荧光素酶报告基因检测分析 BANCR 与 miR-34c 的相互作用。CCK-8 检测分析 BANCR 和 miR-34c 过表达对 HASMCs 增殖的影响。Western blot 检测分析 BANCR 和 miR-34c 过表达对 HMGB1、TNF-ɑ 和 Bcl-2 蛋白表达的影响。本研究发现，动脉粥样硬化中 BANCR 上调，而 miR-34c 下调。生物信息学分析表明，BANCR 和 miR-34c 可以直接相互作用。此外，BANCR 的过表达可以降低 HASMCs 中 miR-34c 的表达，但 miR-34c 的过表达不能影响 BANCR 的表达。此外，BANCR 的过表达增加了 miR-34c 的甲基化，而内源性 BANCR 的敲低降低了 miR-34c 的甲基化。此外，BANCR 的过表达降低了 miR-34c 对 HASMCs 增殖的影响，并逆转了 miR-34c 对 HMGB1、TNF-ɑ 和 Bcl-2 表达的影响。BANCR 的过表达通过下调 miR-34c 的甲基化诱导 HASMCs 增殖。因此，鉴于动脉粥样硬化中 BANCR 的上调，其表达可能被视为动脉粥样硬化预防和预后的一种新的有用的生物标志物。但是，考虑到其他潜在疾病对动脉粥样硬化中 BANCR 表达和 miR-34c 的可能影响，建议进一步研究。
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