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Ning Xu,Aimin Wu,Fuming Li,Hao Lin,Jiada Wu,Peinan Wang,Yuancheng Du,Zhifeng Ying 한국물리학회 2004 THE JOURNAL OF THE KOREAN PHYSICAL SOCIETY Vol.44 No.32
CNx nanocrystals and nanotubes were synthesized on Co/Ni-covered Si(100) wafers using a nitrogen-atom-beam-assisted pulsed laser ablation deposition method. Transimission electron microscopy, X-ray photoelectron spectroscopy and Raman spectroscopy showed that nanometer-sized CNx nanocrystals and nanotubes were contained in the as-deposited lms. The co-catalyzation by the cobalt and nickel in the synthesis process is considered to play an important role in the formation of CNx nanocrystals and nanotubes. The reasons for the formation of CNx nanocrystals and nanotubes have been analyzed.
Wen-Ning Xu,Huo-Liang Zheng,Run-Ze Yang,Tao Liu,Wei Yu,Xin-Feng Zheng,Bo Li,Sheng-Dan Jiang,Lei-Sheng Jiang 생화학분자생물학회 2019 Experimental and molecular medicine Vol.51 No.-
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.