A circular RNA from NFIX facilitates oxidative stress-induced H9c2 cells apoptosis
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A circular RNA from NFIX facilitates oxidative stress-induced H9c2 cells apoptosis Xianglun Cui 1 & Yanhan Dong 2 & Mingyu Li 1 & Xuekang Wang 1 & Meiqing Jiang 1 & Weiwei Yang 1 & Gege Liu 1 & Shuqi Sun 1 & Wenhua Xu 1 Received: 15 December 2019 / Accepted: 11 June 2020 / Editor: Tetsuji Okamoto # The Society for In Vitro Biology 2020
Abstract Myocardial infarction is the leading cause of death worldwide, and cardiomyocyte apoptosis during myocardial infarction and reperfusion is a significant factor of poor prognosis. As important regulatory molecules, biofunctions of circRNAs in the pathogenesis of myocardial infarction remain elusive. To confirm the expression level and biological function of circNFIX in cardiomyocytes upon oxidative stress. Divergent polymerase chain reaction and Sanger sequencing were performed to verify the circular structure. The stability of circNFIX was confirmed by RNase R treatment and actinomycin D assay. In order to simulate oxidative stress during myocardial infarction, H9c2 cells were subjected to hydrogen peroxide and hypoxia stimulation. In vivo, mouse models of myocardial ischemia were established. The biological function of circNFIX in cardiomyocytes was investigated through loss- and gain-of-function assays, and cardiomyocyte apoptosis level was detected by the terminal deoxyribonucleotidyl transferase-mediated TdT-mediated dUTP nick end labeling assay and Western blot. CircNFIX is abundant, conserved, and stable in H9c2 cells. The expression of circNFIX was significantly downregulated in cardiomyocytes subjected to oxidative stress. Enforced CircNFIX promotes H9c2 cells apoptosis induced by hydrogen peroxide, in sharp contrast to circNFIX knockdown. In this study, we found that circNFIX served as a pro-apoptosis factor in cardiomyocyte apoptosis. CircNFIX possesses potential to be the biomarker and therapeutic target in myocardial infarction. Keywords circNFIX . Myocardial infarction . Cardiomyocyte apoptosis . Oxidative stress
Introduction Myocardial infarction (MI), as one of ischemic heart diseases, is the leading cause of morbidity and mortality worldwide (Townsend et al. 2016; Benjamin et al. 2017). With the application of thrombolytic therapy and percutaneous coronary intervention, the blood flow of heart is reperfused, and survival rate of patients with myocardial infarction is significantly Xianglun Cui and Yanhan Dong contributed equally to this work. Electronic supplementary material The online version of this article (https://doi.org/10.1007/s11626-020-00476-z) contains supplementary material, which is available to authorized users. * Wenhua Xu [email protected] 1
Department of Inspection, The Medical Faculty, Qingdao University, Qingdao 266003, China
2
Institute for Translational Medicine, Qingdao University, Deng Zhou Road 38, Qingdao 266021, China
elevated. However, after reperfusion, reactive oxygen species overload and calcium dyshomeostasis in cardiomyocytes can open mitochondrial permeability transition pores, leading to cardiomyocytes apoptosis (Hausenloy
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