miR-190a-5p regulates cardiomyocytes response to ferroptosis via directly targeting GLS2

被引:21
|
作者
Zhou, Xiaodao [1 ]
Zhuo, Mali [2 ]
Zhang, Yayun [2 ]
Shi, Erdong [1 ]
Ma, Xujie [1 ]
Li, Hong [1 ]
机构
[1] Ningbo Yinzhou 2 Hosp, Dept Anesthesiol, Ningbo Urol & Nephrol Hosp, 998 North Qianhe Rd, Ningbo 315100, Zhejiang, Peoples R China
[2] Ningbo Yinzhou 2 Hosp, Dept Clin Pharm, Ningbo Urol & Nephrol Hosp, 998 North Qianhe Rd, Ningbo 315100, Zhejiang, Peoples R China
关键词
Ferroptosis; miR-190a-5p; GLS2; Cardiomyocytes; Myocardial infarction; PATHOPHYSIOLOGY; CARCINOMA; MECHANISM;
D O I
10.1016/j.bbrc.2021.05.100
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Ferroptosis is a novel identified form of regulated cell death that has been implied in the pathology of myocardial infarction (MI). However, the regulation mechanisms of ferroptosis in cardiomyocyte are still elusive. MiRNAs are a group of small non-coding RNAs that play crucial roles in various biological activities. Till now, little is known about the role of miRNA in the ferroptosis of cardiomyocytes. In the current study, we found that miR-190a-5p negatively regulate ferroptosis via directly targeting GLS2 in rat cardiomyocyte H9c2 cells. Forced expression of miR-190a-5p inhibited GLS2, resulting in downregulation of ROS, MDA and Fe2+ accumulation. Meanwhile, inhibition of miR-190a-5p caused upregulation of GLS2, resulting in opposite effects which could be blocked by GLS2 inhibitor compound 968. In summary, our findings suggest that miR-190a-5p plays an essential role in regulation of ferroptosis of cardiomyocytes and suggest a potential therapeutic target for MI. (C) 2021 Elsevier Inc. All rights reserved.
引用
收藏
页码:9 / 15
页数:7
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