Exposure of vital cells to necrotic cell lysates induce the IRE1α branch of the unfolded protein response and cell proliferation

被引:5
作者
Rohne, Philipp [1 ]
Wolf, Steven [1 ,2 ]
Doerr, Carolin [1 ]
Ringen, Julia [1 ]
Holtz, Andrew [1 ]
Gollan, Rene [3 ]
Renner, Benjamin [1 ]
Prochnow, Hans [1 ,4 ]
Baiersdoerfer, Markus [1 ]
Koch-Brandt, Claudia [1 ]
机构
[1] Johannes Gutenberg Univ Mainz, Inst Pharm & Biochem Therapeut Life Sci, Johann Joachim Becherweg 30, D-55128 Mainz, Germany
[2] Univ Chicago, Dept Pathol, 5841 S Maryland Ave, Chicago, IL 60637 USA
[3] Johannes Gutenberg Univ Mainz, Univ Med Ctr Mainz, Dept Neurol, Mainz, Germany
[4] Helmholtz Ctr Infect Res GmbH, Dept Chem Biol, Braunschweig, Germany
关键词
Necrosis; Clusterin; UPR; IRE1a; ERK; mTOR; XBP1; MESSENGER-RNA; CLUSTERIN GENE-EXPRESSION; ER STRESS; APOLIPOPROTEIN-J; HEAT-SHOCK; NECROSIS; DENSITY; RETROTRANSLOCATION; TRANSCRIPTION; INFLAMMATION;
D O I
10.1007/s12192-017-0825-6
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Necrosis is a form of cell death that is detrimental to the affected tissue because the cell ruptures and releases its content (reactive oxygen species among others) into the extracellular space. Clusterin (CLU), a cytoprotective extracellular chaperone has been shown to be upregulated in the face of necrosis. We here show that in addition to CLU upregulation, necrotic cell lysates induce JNK/SAPK signaling, the IRE1 alpha branch of the unfolded protein response (UPR), the MAPK/ERK1/2, and the mTOR signaling pathways and results in an enhanced proliferation of the vital surrounding cells. We name this novel response mechanism: Necrosis-induced Proliferation (NiP).
引用
收藏
页码:77 / 88
页数:12
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