Department of Cardiac Function Room, The First People's Hospital of Lianyungang (Xuzhou Medical University Affiliated Hospital of Lianyungang), Lianyungang, China.
Eur Rev Med Pharmacol Sci. 2019 Oct;23(20):9050-9057. doi: 10.26355/eurrev_201910_19307.
This study aims to clarify the influence of microRNA-410-3p (miRNA-410-3p) on hypoxia-induced injury in cardiomyocytes.
MiRNA-410-3p level, apoptotic rate, and cell viability in AC16 cells undergoing normoxia or hypoxia preconditioning were assessed. The regulatory effects of miRNA-410-3p and TRAF5 on the proliferative and apoptotic abilities of AC16 cells were evaluated. The binding relationship between miRNA-410-3p and TRAF5 was verified by Dual-Luciferase Reporter Gene Assay.
Hypoxia preconditioning triggered apoptosis and inhibited the viability in AC16 cells. MiRNA-410-3p was downregulated in cardiomyocytes under the hypoxic environment. The overexpression of miRNA-410-3p stimulated proliferation and inhibited apoptosis in hypoxia preconditioning AC16 cells. TRAF5 was proved to be the target of miRNA-410-3p. TRAF5 level was negatively regulated by miRNA-410-3p. The silence of TRAF5 could reverse viability and apoptosis changes in hypoxic AC16 cells overexpressing miRNA-410-3p.
MiRNA-410-3p protects hypoxia-induced proliferation suppression and apoptosis stimulation in cardiomyocytes via targeting TRAF5.
本研究旨在阐明 microRNA-410-3p（miRNA-410-3p）对心肌细胞缺氧损伤的影响。
检测 AC16 细胞在常氧或缺氧预处理下的 miRNA-410-3p 水平、凋亡率和细胞活力。评估 miRNA-410-3p 和 TRAF5 对 AC16 细胞增殖和凋亡能力的调节作用。通过双荧光素酶报告基因检测验证 miRNA-410-3p 和 TRAF5 之间的结合关系。
缺氧预处理可诱导 AC16 细胞凋亡并抑制其活力。在缺氧环境下，心肌细胞中的 miRNA-410-3p 表达下调。miRNA-410-3p 的过表达可刺激缺氧预处理 AC16 细胞的增殖并抑制其凋亡。TRAF5 被证实是 miRNA-410-3p 的靶基因。miRNA-410-3p 负调控 TRAF5 水平。沉默 TRAF5 可逆转过表达 miRNA-410-3p 的缺氧 AC16 细胞的活力和凋亡变化。
miRNA-410-3p 通过靶向 TRAF5 保护心肌细胞免受缺氧诱导的增殖抑制和凋亡刺激。
