Emergency Medicine Clinical Research Center, Beijing Chao-Yang Hospital, Capital Medical University, Beijing Key Laboratory of Cardiopulmonary Cerebral Resuscitation, Beijing, China.
Emergency Medicine Clinical Research Center, Beijing Chao-Yang Hospital, Capital Medical University, Beijing Key Laboratory of Cardiopulmonary Cerebral Resuscitation, Beijing, China.
Rev Port Cardiol. 2024 Feb;43(2):77-84. doi: 10.1016/j.repc.2023.04.017. Epub 2023 Aug 29.
The increasing incidence of ischemic heart disease is a serious threat to human health. Increased CASC15, a long non-coding RNA, has been shown to adversely affect cardiac muscle. The objective of this paper was to explore the effect of CASC15 on a cell model of myocardial infarction and its possible mechanism.
H9c2 cells were selected to establish the myocardial infarction model through hypoxia/reoxygenation (H/R) treatment. The expression of CASC15 was attenuated by cell transfection in vitro. The level of CASC15 was detected by RT-qPCR. Cell viability was detected by CCK-8 assay, and cell apoptosis was assessed by flow cytometry. The content of MDA and the activity of SOD and GSH-Px were measured by ELISA. Luciferase reporter gene assay was used to determine the relationship between CASC15 and miRNA.
CASC15 expression was increased in H/R-treated H9c2 cells. Overexpression of CASC15 adversely affected cell viability and promoted H/R-induced oxidative stress. Inhibition of CASC15 promoted cell viability and suppressed cell apoptosis and oxidative stress damage. Additionally, luciferase reporter gene assay confirmed the targeting relationship between CASC15 and miR-542-3p, and attenuating CASC15 expression enhanced the level of miR-542-3p. Reduction of miR-542-3p weakened the viability of the H/R cell model, increased apoptosis, and enhanced oxidative stress damage.
This study suggests that overexpression of CASC15 may inhibit the viability of H9c2 cells, promote apoptosis and induce oxidative stress through targeted regulation of miR-542-3p expression.
缺血性心脏病发病率的增加对人类健康构成了严重威胁。长链非编码 RNA CASC15 的增加已被证明对心肌有不利影响。本文旨在探讨 CASC15 对心肌梗死细胞模型的影响及其可能的机制。
选择 H9c2 细胞通过缺氧/复氧（H/R）处理建立心肌梗死模型。通过细胞转染体外减弱 CASC15 的表达。采用 RT-qPCR 检测 CASC15 水平。CCK-8 法检测细胞活力，流式细胞术检测细胞凋亡。ELISA 法测定 MDA 含量及 SOD、GSH-Px 活性。荧光素酶报告基因实验确定 CASC15 与 miRNA 的关系。
H/R 处理的 H9c2 细胞中 CASC15 表达增加。过表达 CASC15 对细胞活力产生不利影响，并促进 H/R 诱导的氧化应激。抑制 CASC15 促进细胞活力并抑制细胞凋亡和氧化应激损伤。此外，荧光素酶报告基因实验证实了 CASC15 与 miR-542-3p 的靶向关系，减弱 CASC15 表达可增强 miR-542-3p 水平。降低 miR-542-3p 减弱了 H/R 细胞模型的活力，增加了凋亡，并增强了氧化应激损伤。
本研究表明，过表达 CASC15 可能通过靶向调节 miR-542-3p 的表达，抑制 H9c2 细胞的活力，促进凋亡并诱导氧化应激。
