Anisomycin Prevents OGD-induced Necroptosis by Regulating the E3 Ligase CHIP

Overview

Journal Sci Rep

Specialty Science

Date 2018 Apr 25

PMID 29686306

Citations 14

Authors

Mi-Bo Tang

Yu-Sheng Li

Shao-Hua Li

Yuan Cheng

Shuo Zhang

Hai-Yang Luo

Cheng-Yuan Mao

Zheng-Wei Hu

Jonathan C Schisler

Chang-He Shi

Yu-Ming Xu

Affiliations

Soon will be listed here.

Abstract

Necroptosis is an essential pathophysiological process in cerebral ischemia-related diseases. Therefore, targeting necroptosis may prevent cell death and provide a much-needed therapy. Ansiomycin is an inhibitor of protein synthesis which can also activate c-Jun N-terminal kinases. The present study demonstrated that anisomycin attenuated necroptosis by upregulating CHIP (carboxyl terminus of Hsc70-interacting protein) leading to the reduced levels of receptor-interacting protein kinase 1 (RIPK1) and receptor-interacting protein kinase 3 (RIPK3) proteins in two in vitro models of cerebral ischemia. Further exploration in this research revealed that losing neither the co-chaperone nor the ubiquitin E3 ligase function of CHIP could abolish its ability to reduce necroptosis. Collectively, this study identifies a novel means of preventing necroptosis in two in vitro models of cerebral ischemia injury through activating the expression of CHIP, and it may provide a potential target for the further study of the disease.

Citing Articles

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