Autophagy protects against palmitate-induced apoptosis in hepatocytes.
Autophagy protects against palmitate-induced apoptosis in hepatocytes.
复制标题
自噬可防止棕榈酸酯诱导的肝细胞凋亡
DOI：
10.1186/2045-3701-4-28
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发表时间：
2014
影响因子：
7.5
通讯作者：
Wei L
中科院分区：
文献类型：
--
作者：
Cai N;Zhao X;Jing Y;Sun K;Jiao S;Chen X;Yang H;Zhou Y;Wei L
BackgroundNon-alcoholic fatty liver disease, one of the most common liver diseases, has obtained increasing attention. Palmitate (PA)-induced liver injury is considered a risk factor for the development of non-alcoholic fatty liver disease. Autophagy, a cellular degradative pathway, is an important self-defense mechanism in response to various stresses. In this study, we investigated whether autophagy plays a protective role in the progression of PA-induced hepatocytes injury.ResultsAnnexin V-FITC/PI staining by FCM analysis, TUNEL assay and the detection of PARP and cleaved caspase3 expression levels demonstrated that PA treatment prominently induced the apoptosis of hepatocytes. Meanwhile, treatment of PA strongly induced the formation of GFP-LC3 dots, the conversion from LC3I to LC3II, the decrease of p62 protein levels and the increase of autophagosomes. These results indicated that PA also induced autophagy activation. Autophagy inhibition through chloroquine pretreatment or Atg5shRNA infection led to the increase of cell apoptosis after PA treatment. Moreover, induction of autophagy by pretreatment with rapamycin resulted in distinct decrease of PA-induced apoptosis. Therefore, autophagy can prevent hepatocytes from PA-induced apoptosis. In the further study, we explored pathway of autophagy activation in PA-treated hepatocytes. We found that PA activated PKCα in hepatocytes, and had no influence on mammalian target of rapamycin and endoplasmic reticulum stress pathways.ConclusionsThese results demonstrated that autophagy plays a protective role in PA-induced hepatocytes apoptosis. And PA might induce autophagy through activating PKCα pathway in hepatocytes.
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影响因子：
25.7
作者：
Ibrahim SH;Akazawa Y;Cazanave SC;Bronk SF;Elmi NA;Werneburg NW;Billadeau DD;Gores GJ
通讯作者：
Gores GJ
影响因子：
56.9
作者：
Fang, YM;Vilella-Bach, M;Chen, J
通讯作者：
Chen, J
影响因子：
4.8
作者：
Ding, Wen-Xing;Ni, Hong-Min;Yin, Xiao-Ming
通讯作者：
Yin, Xiao-Ming
影响因子：
4.8
作者：
Choi, Sung-E;Lee, Sung-Mi;Kang, Yup
通讯作者：
Kang, Yup
影响因子：
3.8
作者：
Han, Chang Woo;Kang, Eun Sil;Seo, Han Geuk
通讯作者：
Seo, Han Geuk