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学科主题: 临床医学
题名:
Autophagy augmented by troglitazone is independent of EGFR transactivation and correlated with AMP-activated protein kinase signaling
作者: Yan, Jinguo2,3; Yang, Huaiyi4; Wang, Gang1; Sun, Lei5; Zhou, Yuguang2; Guo, Yinglu1; Xi, Zhijun1; Jiang, Xuejun2
关键词: PPAR gamma ligand ; autophagy ; p62 ; EGFR ; AMPK
刊名: AUTOPHAGY
发表日期: 2010
卷: 6, 期:1, 页:67-73
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Cell Biology
研究领域[WOS]: Cell Biology
关键词[WOS]: GROWTH-FACTOR RECEPTOR ; MATURATION STEP ; CELL-DEATH ; MTOR ; MACROAUTOPHAGY ; DEGRADATION ; P62/SQSTM1 ; HUNTINGTIN ; SURVIVAL ; DISEASE
英文摘要:

Troglitazone is a synthetic ligand of peroxisome proliferators activated receptor-gamma (PPAR gamma) and induces apoptosis in a variety of malignant cells. However, the underlying mechanism of its regulatory role in macroautophagy (hereafter autophagy) remains largely unknown. Using fluorescence and electron microscopy, we observed that autophagosomes could be induced and identified upon troglitazone challenge in both primary and epidermal growth factor receptor (EGFR)-expressed porcine aortic endothelial (PAE) cells. We report here that troglitazone augments AMP-activated protein kinase-alpha (AMPK alpha) phosphorylation, reduces p70S6 kinase phosphorylation and stimulates autophagy that is independent of EGFR expression and transactivation. Troglitazone stimulus reduced neither lysosomal staining nor GFP-LC3 dots of HeLa cells, when the cells pretreated with AG1478, a specific EGFR kinase inhibitor. Furthermore, AG1478 additively enhanced the troglitazone-induced degradation of sequestosome 1 (SQSTM1/p62), which is a selective substrate of autophagy. Inhibition of AMPK alpha activity either by compound C or by RNA interference markedly reduced the accumulation of microtubule-associated protein 1 light chain 3-II (LC3-II), a good indicator of autophagy; whereas blockage of PPAR gamma activity by the irreversible antagonist GW9662 or by overexpressing dominate-negative PPAR gamma did not affect LC3-II accumulation and AMPK phosphorylation. Taken together, we demonstrate that autophagy promoted via troglitazone is correlated with AMPK alpha activation and independent of PPAR gamma activation and EGFR transactivation.

语种: 英语
所属项目编号: 90408024 ; 30470855 ; 30571853 ; 30872588
项目资助者: National Natural Science Foundation of China (NSFC)
WOS记录号: WOS:000276197900008
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/61072
Appears in Collections:北京大学第一临床医学院_泌尿外科_期刊论文

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作者单位: 1.Peking Univ, Inst Urol, Hosp 1, Beijing 100871, Peoples R China
2.Chinese Acad Sci, Biol Resource Ctr, Inst Microbiol, Beijing, Peoples R China
3.Chinese Acad Sci, Grad Sch, Beijing, Peoples R China
4.Chinese Acad Sci, Key Lab Pathogen Microbiol & Immunol, Inst Microbiol, Beijing, Peoples R China
5.Chinese Acad Sci, Inst Biophys, Natl Lab Biomacromol, Ctr Biol Electron Microscopy, Beijing 100080, Peoples R China

Recommended Citation:
Yan, Jinguo,Yang, Huaiyi,Wang, Gang,et al. Autophagy augmented by troglitazone is independent of EGFR transactivation and correlated with AMP-activated protein kinase signaling[J]. AUTOPHAGY,2010,6(1):67-73.
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