Autophagy Mediates HBx-Induced Nuclear Factor-kappa B Activation and Release of IL-6, IL-8, and CXCL2 in Hepatocytes
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摘要Hepatitis B virus (HBV) and one of its encoded proteins, HBV X protein (HBx), have been shown to induce autophagy in hepatoma cells. Substantial evidence indicates that autophagy is a potent suppressor of inflammation. However, sporadic reports suggest that autophagy could promote pro-inflammatory cytokine expression and inflammation in some biological contexts. Here, we show that overexpression of HBx induces LC3B-positive autophagosome formation, increases autophagic flux and enhances the expression of ATG5, ATG7, and LC3B-II in normal hepatocytes. Abrogation of autophagy by small interfering RNA against ATG5 and ATG7 prevents HBx-induced formation of autophagosomes. Autophagy inhibition also abrogates HBx-induced activation of nuclear factor-kappa B (NF-kappa B) and production of interleukin-6 (IL-6), IL-8, and CXCL2. These findings suggest that autophagy is required for HBx-induced NF-kappa B activation and pro-inflammatory cytokine production and could shed new light on the complex role of autophagy in the modulation of inflammation. (C) 2015 Wiley Periodicals, Inc.
著者Luo MXM, Wong SH, Chan MTV, Le Yu L, Yu SSB, Wu F, Xiao ZG, Wang XJ, Zhang L, Cheng ASL, Ng SSM, Chan FKL, Cho CH, Yu J, Sung JJY, Wu WKK
期刊名稱Journal of Cellular Physiology
出版年份2015
月份10
日期1
卷號230
期次10
出版社WILEY-BLACKWELL
頁次2382 - 2389
國際標準期刊號0021-9541
電子國際標準期刊號1097-4652
語言英式英語
Web of Science 學科類別Cell Biology; Physiology

上次更新時間 2020-14-09 於 02:16