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Melatonin prevents nitric oxide-induced apoptosis by increasing the interaction between 14-3-3beta and p-Bad in SK-N-MC cells

Authors
 Seung-Il Choi  ;  Seong-Soo Joo  ;  Yeong-Min Yoo 
Citation
 JOURNAL OF PINEAL RESEARCH, Vol.44(1) : 95-100, 2008 
Journal Title
 JOURNAL OF PINEAL RESEARCH 
ISSN
 0742-3098 
Issue Date
2008
MeSH
14-3-3 Proteins/metabolism* ; Apoptosis/drug effects* ; Cell Line, Tumor ; Humans ; Melatonin/pharmacology* ; Nitric Oxide/adverse effects ; Proto-Oncogene Proteins c-akt/metabolism* ; Signal Transduction/drug effects ; bcl-Associated Death Protein/metabolism*
Keywords
Akt/PKB ; Bad ; GSK3 a/b ; melatonin ; SK-N-MC ; SNAP ; 14-3-3b
Abstract
The anti-apoptotic effect of melatonin has been described in vivo and in vitro. A previous report has revealed that melatonin suppresses nitric oxide (NO)-induced apoptosis via the induction of Bcl-2 expression in PGT-beta pineal cells. To investigate the protective mechanism of melatonin on NO donor S-nitroso-N-acetyl-penicillamine (SNAP)-induced apoptosis, we examined the anti-apoptotic upstream signaling pathway of Bcl-2 in the human neuroblastoma cell line SK-N-MC. The flow cytometry results revealed that apoptosis occurred in NO-treated cells, while cell death was inhibited by pretreatment with melatonin (100 microm). In addition, decreased Bax expression, increased Bcl-2 expression and a decreased release of cytochrome c into the cytosol were observed in the melatonin-pretreated SK-N-MC cells. We also found that melatonin treatment induced the activation of Akt/PKB and the phosphorylation of GSK3alpha/beta and Bad. Furthermore, melatonin treatment not only increased the protein-protein interactions between 14-3-3beta and p-Bad, but also decreased the release of cytochrome c from mitochondria into the cytosol. In summary, the protective effect of melatonin against NO-induced apoptosis was mediated by the inhibition of Bad translocation from the cytosol to the mitochondria by the induction of protein-protein interactions between 14-3-3beta and p-Bad
Full Text
http://onlinelibrary.wiley.com/doi/10.1111/j.1600-079X.2007.00494.x/abstract
DOI
10.1111/j.1600-079X.2007.00494.x
Appears in Collections:
5. Research Institutes (연구소) > Corneal Dystrophy Research Institute (각막이상증연구소) > 1. Journal Papers
Yonsei Authors
Choi, Seung Il(최승일) ORCID logo https://orcid.org/0000-0001-7168-8795
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/111144
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