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Mitochondrial NDUFA4L2 attenuates the apoptosis of nucleus pulposus cells induced by oxidative stress via the inhibition of mitophagy
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Mitochondrial NDUFA4L2 attenuates the apoptosis of nucleus pulposus cells induced by oxidative stress via the inhibition of mitophagy
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Journal Article
Mitochondrial NDUFA4L2 attenuates the apoptosis of nucleus pulposus cells induced by oxidative stress via the inhibition of mitophagy
2019
Overview
The main pathological mechanism of intervertebral disc degeneration (IVDD) is the programmed apoptosis of nucleus pulposus (NP) cells. Oxidative stress is a significant cause of IVDD. Whether mitophagy is induced by strong oxidative stress in IVDD remains to be determined. This study aimed to investigate the relationship between oxidative stress and mitophagy and to better understand the mechanism of IVDD in vivo and in vitro. To this end, we obtained primary NP cells from the human NP and subsequently exposed them to TBHP. We observed that oxidative stress induced mitophagy to cause apoptosis in NP cells, and we suppressed mitophagy and found that NP cells were protected against apoptosis. Interestingly, TBHP resulted in mitophagy through the inhibition of the HIF-1α/NDUFA4L2 pathway. Therefore, the upregulation of mitochondrial NDUFA4L2 restricted mitophagy induced by oxidative stress. Furthermore, the expression levels of HIF-1α and NDUFA4L2 were decreased in human IVDD. In conclusion, these results demonstrated that the upregulation of NDUFA4L2 ameliorated the apoptosis of NP cells by repressing excessive mitophagy, which ultimately alleviated IVDD. These findings show for the first time that NDUFA4L2 and mitophagy may be potential therapeutic targets for IVDD.
Disc degeneration: Mitochondria at the root of the problem
A study in rats highlights the role of mitochondria in intervertebral disc degeneration (IVDD), one of the most important and prevalent predisposing factors for lower back pain. Previous studies have shown that in IVDD, oxidative stress results in the gradual loss of cells in the inner part of vertebral discs which cushion the space between vertebrae. Sheng-Dan Jiang and Lei-Sheng Jiang at Shanghai Jiaotong University School of Medicine found that oxidative stress in these cells causes the selective degradation of mitochondria by preventing the expression of a protein that is essential for mitochondrial function. Overexpressing this protein in the intervertebral discs of rats with IVDD alleviated degeneration, suggesting that restoring mitochondrial function could be an effective therapeutic strategy for easing the pain associated with the condition.
Publisher
Nature Publishing Group UK,Springer Nature B.V,생화학분자생물학회
Subject
/ 13/2
/ 14/1
/ 38/1
/ 38/89
/ 42/44
/ 59/57
/ Animals
/ Biomedical and Life Sciences
/ Chromatin Immunoprecipitation
/ Electron Transport Complex I - genetics
/ Electron Transport Complex I - metabolism
/ Male
/ Membrane Potential, Mitochondrial
/ Microscopy, Electron, Transmission
/ Nucleus Pulposus - metabolism
/ Oxidative Stress - physiology
/ Rats
/ RNA, Small Interfering - genetics
/ RNA, Small Interfering - metabolism
/ 생화학
