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学科主题: 临床医学
题名:
PARP and RIP-1 are required for autophagy induced by 11 ′-deoxyverticillin A, which precedes caspase-dependent apoptosis
作者: Zhang, Nan6; Chen, Yali1; Jiang, Ruixuan4; Li, Erwei1; Chen, Xiuling2; Xi, Zhijun6; Guo, Yinglu6; Liu, Xingzhong1; Zhou, Yuguang2,3; Che, Yongsheng1,5; Jiang, Xuejun1,2
关键词: 11 &prime ; -deoxyverticillin A ; autophagy ; apoptosis ; PARP ; RIP
刊名: AUTOPHAGY
发表日期: 2011-06-01
DOI: 10.4161/auto.7.6.15103
卷: 7, 期:6, 页:598-612
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]: NECROTIC CELL-DEATH ; POLY(ADP-RIBOSE) POLYMERASE-1 ; MONITORING AUTOPHAGY ; MEDIATED CLEAVAGE ; REDOX REGULATION ; SELF-DIGESTION ; DNA-DAMAGE ; HELA-CELLS ; SURVIVAL ; DEGRADATION
英文摘要:

The epipolythiodioxopiperazines (ETPs) are fungal secondary metabolites proven to trigger both apoptotic and necrotic cell death of tumor cells. However, the underlying mechanism of their regulatory role in macroautophagy and the interplay between autophagy and apoptosis initiated by the ETPs, remain unexplored. In the current work, we found that 11′-deoxyverticillin A (C42), a member of the ETPs, induces autophagosome formation, accumulation of microtubule-associated protein 1 light chain 3-II (LC3-II) and degradation of sequestosome 1 (SQSTM1/p62). In addition, the LC3-II accrual and p62 degradation occur prior to caspase activation and coincide with PARP activation. Inhibition of autophagy by either chemical inhibitors or by RNA interference single knockdown of essential autophagic genes partially reduces the cell death and the cleavage of both caspase 3 and PARP. Necrostatin-1, a specific inhibitor of necroptosis, inhibits both the augmentation of LC3-II and the cleavage of caspase 3, which was confirmed by depletion of receptor-interacting protein 1 (RIP-1), a crucial necrostatin-1-targeted adaptor kinase mediating cell death and survival. Moreover, inhibition of PARP by either chemical inhibitors or RNA interference provides obvious protection for cell viability and suppresses the LC3-II accretion caused by C42 treatment. Interestingly, double silencing of LC3 and p62 completely suppressed PARP cleavage and concurrently and maximally augmented the PAR formation induced by C42. Collectively, we have demonstrated that C42 enhances the cellular autophagic process, which requires both PARP and RIP-1 participation, preceding and possibly augmenting, the caspase-dependent apoptotic cell death.

语种: 英语
所属项目编号: 90408024 ; 30900731 ; 30672097 ; 30870057 ; 30925039 ; 2009CB522302 ; 2009ZX09302-004
项目资助者: National Natural Science Foundation of China (NSFC) ; Ministry of Science and Technology of China
WOS记录号: WOS:000291153300005
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/61867
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.Chinese Acad Sci, Key Lab Systemat Mycol & Lichenol, Beijing, Peoples R China
2.Chinese Acad Sci, Biol Resource Ctr, Beijing, Peoples R China
3.Chinese Acad Sci, Inst Microbiol, State Key Lab Microbial Resources, Beijing, Peoples R China
4.Capital Med Univ, Beijing, Peoples R China
5.Beijing Inst Pharmacol & Toxicol, Beijing, Peoples R China
6.Peking Univ, Hosp 1, Inst Urol, Natl Res Ctr Urol Canc, Beijing 100871, Peoples R China

Recommended Citation:
Zhang, Nan,Chen, Yali,Jiang, Ruixuan,et al. PARP and RIP-1 are required for autophagy induced by 11 ′-deoxyverticillin A, which precedes caspase-dependent apoptosis[J]. AUTOPHAGY,2011,7(6):598-612.
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