PMID- 29844315
OWN - NLM
STAT- MEDLINE
DCOM- 20191210
LR  - 20191217
IS  - 2041-4889 (Electronic)
VI  - 9
IP  - 6
DP  - 2018 May 29
TI  - The kinase receptor-interacting protein 1 is required for inflammasome activation 
      induced by endoplasmic reticulum stress.
PG  - 641
LID - 10.1038/s41419-018-0694-7 [doi]
LID - 641
AB  - Endoplasmic reticulum (ER) stress contributes to the development and progression 
      of many chronic inflammatory diseases, including type 2 diabetes, obesity, 
      atherosclerosis, neurodegenerative diseases, and cancer. ER stress has been 
      reported to induce inflammasome activation and release of mature IL-1beta, which 
      contributes to many inflammatory diseases. The molecular mechanisms that activate 
      the inflammasome during ER stress are still poorly understood. Here we report 
      that the kinase receptor-interacting protein 1 (RIP1) plays an important role in 
      ER stress-induced activation of inflammasome. Inhibition of RIP1 kinase activity 
      by Necrostatin-1 or siRNA-mediated RIP1 knockdown significantly reduced ER 
      stress-induced caspase-1 cleavage and IL-1beta secretion in both bone marrow-derived 
      macrophages (BMDMs) and J774A.1 macrophages. We speculate that the mitochondria 
      fission factor dynamin-related protein 1 (DRP1) and reactive oxygen species (ROS) 
      might function as the effectors downstream of RIP1 to mediate inflammasome 
      activation. Our study reveals a critical role for RIP1 in regulating ER 
      stress-induced inflammation responses, and proposes RIP1 as a potential 
      pharmaceutical target to treat diseases resulting from unresolved ER 
      stress-related inflammation.
FAU - Tao, Liang
AU  - Tao L
AD  - Center for Molecular Metabolism, Nanjing University of Science & Technology, 200 
      Xiaolingwei Street, Nanjing, 210094, China.
FAU - Lin, Hongfa
AU  - Lin H
AD  - Center for Molecular Metabolism, Nanjing University of Science & Technology, 200 
      Xiaolingwei Street, Nanjing, 210094, China.
FAU - Wen, Jingjing
AU  - Wen J
AD  - Center for Molecular Metabolism, Nanjing University of Science & Technology, 200 
      Xiaolingwei Street, Nanjing, 210094, China.
FAU - Sun, Qi
AU  - Sun Q
AD  - Center for Molecular Metabolism, Nanjing University of Science & Technology, 200 
      Xiaolingwei Street, Nanjing, 210094, China.
FAU - Gao, Yan
AU  - Gao Y
AD  - Center for Molecular Metabolism, Nanjing University of Science & Technology, 200 
      Xiaolingwei Street, Nanjing, 210094, China.
FAU - Xu, Xi
AU  - Xu X
AD  - Center for Molecular Metabolism, Nanjing University of Science & Technology, 200 
      Xiaolingwei Street, Nanjing, 210094, China.
FAU - Wang, Junsong
AU  - Wang J
AD  - Center for Molecular Metabolism, Nanjing University of Science & Technology, 200 
      Xiaolingwei Street, Nanjing, 210094, China.
FAU - Zhang, Jianfa
AU  - Zhang J
AD  - Center for Molecular Metabolism, Nanjing University of Science & Technology, 200 
      Xiaolingwei Street, Nanjing, 210094, China.
FAU - Weng, Dan
AU  - Weng D
AD  - Center for Molecular Metabolism, Nanjing University of Science & Technology, 200 
      Xiaolingwei Street, Nanjing, 210094, China. danweng@njust.edu.cn.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20180529
PL  - England
TA  - Cell Death Dis
JT  - Cell death & disease
JID - 101524092
RN  - 0 (Inflammasomes)
RN  - 0 (RNA, Small Interfering)
RN  - 0 (Reactive Oxygen Species)
RN  - 20350-15-6 (Brefeldin A)
RN  - EC 2.7.11.1 (Receptor-Interacting Protein Serine-Threonine Kinases)
RN  - EC 2.7.11.1 (Ripk1 protein, mouse)
RN  - EC 2.7.11.1 (Ripk3 protein, mouse)
RN  - EC 3.6.5.5 (Dynamins)
SB  - IM
MH  - Animals
MH  - Apoptosis/drug effects
MH  - Brefeldin A/pharmacology
MH  - Cell Line
MH  - Dynamins/metabolism
MH  - *Endoplasmic Reticulum Stress/drug effects
MH  - Gene Silencing/drug effects
MH  - Inflammasomes/*metabolism
MH  - Mice, Inbred C57BL
MH  - RNA, Small Interfering/metabolism
MH  - Reactive Oxygen Species/metabolism
MH  - Receptor-Interacting Protein Serine-Threonine Kinases/deficiency/*metabolism
PMC - PMC5974395
COIS- The authors declare that they have no conflict of interest.
EDAT- 2018/05/31 06:00
MHDA- 2019/12/18 06:00
PMCR- 2018/05/29
CRDT- 2018/05/31 06:00
PHST- 2017/12/17 00:00 [received]
PHST- 2018/05/09 00:00 [accepted]
PHST- 2018/05/07 00:00 [revised]
PHST- 2018/05/31 06:00 [entrez]
PHST- 2018/05/31 06:00 [pubmed]
PHST- 2019/12/18 06:00 [medline]
PHST- 2018/05/29 00:00 [pmc-release]
AID - 10.1038/s41419-018-0694-7 [pii]
AID - 694 [pii]
AID - 10.1038/s41419-018-0694-7 [doi]
PST - epublish
SO  - Cell Death Dis. 2018 May 29;9(6):641. doi: 10.1038/s41419-018-0694-7.