Modulation of Atg5 expression by globular adiponectin contributes to autophagy flux-and suppression of ethanol-induced cell death in liver cells

Title
Modulation of Atg5 expression by globular adiponectin contributes to autophagy flux-and suppression of ethanol-induced cell death in liver cells
Author(s)
최동영사로즈네팔김미진이응석김정애손동환[손동환]이성희[이성희]송경[송경]김상현[김상현]정길생[정길생]정태천박필훈
Keywords
ACTIVATED PROTEIN-KINASE; INDUCED APOPTOSIS; HEPG2 CELLS; FATTY LIVER; DISEASES; STRESS; DEGRADATION; INHIBITION; P62/SQSTM1; CROSSTALK
Issue Date
201406
Publisher
PERGAMON-ELSEVIER SCIENCE LTD
Citation
FOOD AND CHEMICAL TOXICOLOGY, v.68, pp.11 - 22
Abstract
Globular adiponectin (gAcrp) protects liver cells from ethanol-induced apoptosis via induction of autophagy. However, the underlying mechanisms are unknown. The present study aims to investigate the potential role of autophagy-related protein 5 (Atg5), an essential Atg for the elongation of autophagosomes, in suppression of ethanol-induced cytotoxicity by gAcrp. Here, we demonstrated that suppression of Atg5 expression by ethanol was restored by pretreatment with gAcrp both in primary rat hepatocytes and human hepatoma cell line (HepG2). Moreover, ethanol-induced accumulation of p62 (sequestosomel), a marker of autophagic flux, was restored by gAcrp treatment, implying that gAcrp modulates autophagic flux in liver cells. Further, Atg5 silencing prevented p62 degradation by gAcrp, suggesting that Atg5 plays a critical role in induction of autophagic flux by gAcrp. Interestingly, gene silencing of Atg5 by siRNA abrogated restoration of autophagosome formation by gAcrp in ethanol-treated cells. Finally, protection of liver cells by gAcrp from ethanol-induced apoptosis was also significantly attenuated by knocking-down of Atg5 expression, suggesting an important role of Atg5 in autophagy induction and cellular apoptosis modulated by gAcrp. Taken together, our data demonstrated that Atg5 expression, at least in part, is implicated in gAcrp-induced autophagy and subsequent anti-apoptotic effects in ethanol-treated liver cells. (C) 2014 Elsevier Ltd. All rights reserved.
URI
http://hdl.handle.net/YU.REPOSITORY/31986http://dx.doi.org/10.1016/j.fct.2014.02.027
ISSN
0278-6915
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약학대학 > 약학부 > Articles
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