Department of Cardiology, The Second Affiliated Hospital (Jiande Branch), Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Department of Nephrology, The Second Affiliated Hospital (Jiande Branch), Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
J Biochem Mol Toxicol. 2022 Oct;36(10):e23159. doi: 10.1002/jbt.23159. Epub 2022 Jul 25.
MicroRNAs (miRNAs) feature prominently in regulating the progression of chronic heart failure (CHF). This study was performed to investigate the role of miR-8485 in the injury of cardiomyocytes and CHF. It was found that miR-8485 level was markedly reduced in the plasma of CHF patients, compared with the healthy controls. H O treatment increased tumor necrosis factor-α, interleukin (IL)-6, and IL-1β levels, inhibited the viability of human adult ventricular cardiomyocyte cell line AC16, and increased the apoptosis, while miR-8485 overexpression reversed these effects. Tumor protein p53 inducible nuclear protein 1 (TP53INP1) was identified as a downstream target of miR-8485, and TP53INP1 overexpression weakened the effects of miR-8485 on cell viability, apoptosis, as well as inflammatory responses. Our data suggest that miR-8485 attenuates the injury of cardiomyocytes by targeting TP53INP1, suggesting it is a protective factor against CHF.
微小 RNA(miRNAs)在调控慢性心力衰竭(CHF)的进展中起着重要作用。本研究旨在探讨 miR-8485 在心肌细胞损伤和 CHF 中的作用。研究发现,与健康对照组相比,CHF 患者血浆中的 miR-8485 水平明显降低。HO 处理增加了肿瘤坏死因子-α、白细胞介素(IL)-6 和 IL-1β 的水平,抑制了人成体心室肌细胞系 AC16 的活力,并增加了细胞凋亡,而过表达 miR-8485 则逆转了这些作用。肿瘤蛋白 p53 诱导核蛋白 1(TP53INP1)被鉴定为 miR-8485 的下游靶标,过表达 TP53INP1 削弱了 miR-8485 对细胞活力、凋亡和炎症反应的作用。我们的数据表明,miR-8485 通过靶向 TP53INP1 减轻心肌细胞损伤,表明其是 CHF 的一种保护因素。