Journal
JOURNAL OF MOLECULAR NEUROSCIENCE
Volume 63, Issue 2, Pages 142-151Publisher
HUMANA PRESS INC
DOI: 10.1007/s12031-017-0964-3
Keywords
Mild hypothermia; RBM3; Apoptosis; UV irradiation; Signaling pathways; Neuroprotection
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Funding
- National Natural Science Foundation of China [81771336]
- Henan Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine [XTCX-2015-ZD3]
- Disciplinary group of Psychology and Neuroscience of Xinxiang Medical University
- Henan Key Laboratory of Biological Psychiatry [ZDSYS2015005]
- Graduate Scientific Research Innovation Support Project of Xinxiang Medical University [YJSCX201649Y]
- Henan Program for Science and Technology Development [162102310490]
- Henan Educational Committee Program for Science and Technology Development of Universities [16A180015]
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Induced by hypothermia, cold-inducible protein RBM3 (RNA-binding protein motif 3), has been implicated in neuroprotection against various toxic insults such as hypoxia and ischemia. However, whether mild hypothermia and RBM3 prevent neural cells from UV irradiation-elicited apoptosis is unclear. In the present study, human neuroblastoma cell line SH-SY5Y was used as a cell model for neural cell death, and it was demonstrated that mild hypothermia protects SH-SY5Y cells from UV irradiation-induced apoptosis. However, the protective effect of mild hypothermia was abrogated when RBM3 was silenced. Conversely, the overexpression of RBM3 rescued SH-SY5Y cells from UV-induced apoptosis, as indicated by the decreased levels of cleaved caspase-3 and PARP, and increased cell survival. The analysis on the mechanism underlying RBM3-mediated neuroprotection against UV insult showed that RBM3 could substantially block the activation of p38 and JNK signaling pathways. In addition, the overexpression of RBM3 reduced the expression of pro-apoptotic proteins Bax and Bad, leaving the pro-survival protein Bcl-2 unaffected. In conclusion, RBM3 is the key mediator of mild hypothermia-related protection against UV in neuroblastoma cells, and the neuroprotective effect might be exerted through interfering with pro-apoptotic signaling pathways p38 and JNK and regulating pro-apoptotic proteins Bax and Bad.
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