Effects of NRF-1 and PGC-1α cooperation on HIF-1α and rat cardiomyocyte apoptosis under hypoxia

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]
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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