生物
缺氧(环境)
细胞凋亡
细胞生物学
HIF1A型
转录因子
缺氧诱导因子
辅活化剂
受体
缺氧诱导因子1
癌症研究
基因
生物化学
血管生成
化学
有机化学
氧气
作者
Nan Niu,Hui Li,Xiancai Du,Chan Wang,Junliang Li,Ji‐Hui Yang,Cheng Liu,Songhao Yang,Yazhou Zhu,Wei Zhao
出处
期刊:Gene
[Elsevier BV]
日期:2022-05-13
卷期号:834: 146565-146565
被引量:11
标识
DOI:10.1016/j.gene.2022.146565
摘要
Hypoxia is a primary inducer of cardiomyocyte injury, its significant marker being hypoxia-induced cardiomyocyte apoptosis. Nuclear respiratory factor-1 (NRF-1) and hypoxia-inducible factor-1α (HIF-1α) are transcriptional regulatory elements implicated in multiple biological functions, including oxidative stress response. However, their roles in hypoxia-induced cardiomyocyte apoptosis remain unknown. The effect HIF-1α, together with NRF-1, exerts on cardiomyocyte apoptosis also remains unclear.We established a myocardial hypoxia model and investigated the effects of these proteins on the proliferation and apoptosis of rat cardiomyocytes (H9C2) under hypoxia. Further, we examined the association between NRF-1 and HIF-1α to improve the current understanding of NRF-1 anti-apoptotic mechanisms.The results show that NRF-1 and HIF-1α are important anti-apoptotic molecules in H9C2 cells under hypoxia, although their regulatory mechanisms differ. NRF-1 could bind to the promoter region of Hif1a and negatively regulate its expression. Additionally, HIF-1β exhibited competitive binding with NRF-1 and HIF-1α, demonstrating a synergism between NRF-1 and the peroxisome proliferator-activated receptor-gamma coactivator-1α.These results indicate that cardiomyocytes can regulate different molecular patterns to tolerate hypoxia, providing a novel methodological framework for studying cardiomyocyte apoptosis under hypoxia.
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