NDLI: SHP-2 phosphatase controls aryl hydrocarbon receptor-mediated ER stress response in mast cells

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SHP-2 phosphatase controls aryl hydrocarbon receptor-mediated ER stress response in mast cells

Content Provider	Springer Nature Link
Author	Wang, Hsueh Chun Zhou, Yufeng Huang, Shau Ku
Copyright Year	2016
Abstract	Previously we reported that exposure of mouse and human mast cells to aryl hydrocarbon receptor (AhR) ligands resulted in reactive oxygen species (ROS)- and calcium (Ca2+)-dependent activation of mast cells in vitro and in vivo. However, the mechanisms through which the AhR-ligand axis mediates stress response, Ca2+ signaling and subsequent mast cell activation remain to be fully elucidated. Evidence is provided herein that SHP-2 is critical in regulating AhR-mediated ER stress response and intracellular Ca2+ dynamics. We found that an AhR ligand, FICZ, induced significant reduction of intracellular GSH and an increased level of intracellular ROS. Significantly, we showed that in FICZ-treated mast cells, SHP-2 promoted, in a ROS-dependent manner, ER stress response involving primarily the PERK signaling pathway, ATF4 activation and eIF2α phosphorylation, which could be reversed by the addition of an antioxidant, NAC, and was inhibited in cells with SHP-2 knockdown. Our findings suggested that SHP-2 is critical in controlling ER stress signals in response to AhR activation, which provides a new mechanistic insight into how the AhR-ligand axis regulates cellular adaptation to the environmental insult in mast cells.
Starting Page	1739
Ending Page	1748
Page Count	10
File Format	PDF
ISSN	03405761
Journal	Archives of Toxicology
Volume Number	91
Issue Number	4
e-ISSN	14320738
Language	English
Publisher	Springer Berlin Heidelberg
Publisher Date	2016-10-05
Publisher Place	Berlin, Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Aryl hydrocarbon receptor Mast cells ER stress Src-homology 2 domain-containing tyrosine phosphatase Pharmacology/Toxicology Occupational Medicine/Industrial Medicine Environmental Health Biomedicine
Content Type	Text
Resource Type	Article
Subject	Health, Toxicology and Mutagenesis Medicine Toxicology

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