学科主题临床医学
Autophagy augmented by troglitazone is independent of EGFR transactivation and correlated with AMP-activated protein kinase signaling
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
2010
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
WOS记录号WOS:000276197900008
项目编号90408024 ; 30470855 ; 30571853 ; 30872588
资助机构National Natural Science Foundation of China (NSFC)
引用统计
被引频次:27[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/61072
专题北京大学第一临床医学院_北京大学泌尿外科研究所
北京大学第一临床医学院_泌尿外科
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
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GB/T 7714
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.
APA Yan, Jinguo.,Yang, Huaiyi.,Wang, Gang.,Sun, Lei.,Zhou, Yuguang.,...&Jiang, Xuejun.(2010).Autophagy augmented by troglitazone is independent of EGFR transactivation and correlated with AMP-activated protein kinase signaling.AUTOPHAGY,6(1),67-73.
MLA Yan, Jinguo,et al."Autophagy augmented by troglitazone is independent of EGFR transactivation and correlated with AMP-activated protein kinase signaling".AUTOPHAGY 6.1(2010):67-73.
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