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NAF‐1 antagonizes starvation‐induced autophagy through AMPK signaling pathway in cardiomyocytes
Author(s) -
Du Xiaohong,
Xiao Renjie,
Xiao Fan,
Chen Yong,
Hua Fuzhou,
Yu Shuchun,
Xu Guohai
Publication year - 2015
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.10453
Subject(s) - autophagy , ampk , microbiology and biotechnology , starvation , ectopic expression , chemistry , programmed cell death , cell , immunoprecipitation , biology , endocrinology , gene , apoptosis , biochemistry , phosphorylation , protein kinase a
NAF‐1 (nutrient‐deprivation autophagy factor‐1), an autophagy‐related gene‐related (ATG) protein, has been implicated in the autophagic pro‐survival response. However, its role in autophagy has not been examined in the cardiomyocytes. In this study, we found that nutritional stress (NS) induced by glucose deprivation strongly induced autophagy in cultured neonatal rat cardiomyocytes, which was associated with NAF‐1 down‐regulation in cardiomyocytes under NS conditions. Furthermore, we demonstrate that ectopic expression of NAF‐1 was sufficient to inhibit autophagy in cardiomyocytes under glucose deprivation conditions. Moreover, results of the co‐immunoprecipitation assay indicate that NAF‐1 antagonized autophagy by promoting the interaction between Beclin1 and Bcl‐2 in NS‐induced cardiomyocytes. Importantly, our results indicate that overexpression of NAF‐1 significantly inhibited AMPK activity and protected cardiomyocytes from NS‐induced cell death. Taken together, these data show that ectopic expression of NAF‐1 antagonizes the degree of autophagy in cardiomyocytes and enhances cell survival during starvation conditions.