Effects of nuclear respiratory factor-1 on apoptosis and mitochondrial dysfunction induced by cobalt chloride in H9C2 cells
Effects of nuclear respiratory factor-1 on apoptosis and mitochondrial dysfunction induced by cobalt chloride in H9C2 cells
复制标题
核呼吸因子1对氯化钴诱导的H9C2细胞凋亡和线粒体功能障碍的影响
DOI：
10.3892/mmr.2019.9839
复制
发表时间：
2019-03-01
影响因子：
3.4
通讯作者：
Song, Rong
中科院分区：
文献类型：
--
作者：
Niu, Nan;Li, Zihua;Song, Rong
Hypoxia-induced apoptosis occurs in various diseases. Cobalt chloride (CoCl2) is a hypoxia mimic agent that is frequently used in studies investigating the mechanisms of hypoxia. Nuclear respiratory factor-1 (NRF-1) is a transcription factor with an important role in the expression of mitochondrial respiratory and mitochondria-associated genes. However, few studies have evaluated the effects of NRF-1 on apoptosis, particularly with regard to damage caused by CoCl2. In the present study, the role of NRF-1 in mediating CoCl2-induced apoptosis was investigated using cell viability analysis, flow cytometry, fluorescence imaging, western blotting analysis, energy metabolism analysis and reverse transcription-quantitative polymerase chain reaction. The present results revealed that the apoptosis caused by CoCl2 could be alleviated by NRF-1. Furthermore, overexpression of NRF-1 increased the expression of B-cell lymphoma-2, hypoxia inducible factor-1 and NRF-2. Also, cell damage induced by CoCl2 may be associated with depolarization of mitochondrial membrane potential, and NRF-1 suppressed this effect. Notably, the oxygen consumption rate (OCR) was reduced in CoCl2-treated cells, whereas overexpression of NRF-1 enhanced the OCR, suggesting that NRF-1 had protective effects. In summary, the present study demonstrated that NRF-1 protected against CoCl2-induced apoptosis, potentially by strengthening mitochondrial function to resist CoCl2-induced damage to H9C2 cells. The results of the present study provide a possible way for the investigation of myocardial diseases.
