Glutathione transferase Omega 1 is required for the lipopolysaccharide- stimulated induction of NADPH oxidase 1 and the production of reactive oxygen species in macrophages

Menon, Deepthi, Coll, Rebecca, O'Neill, Luke A. J. and Board, Philip G. (2014) Glutathione transferase Omega 1 is required for the lipopolysaccharide- stimulated induction of NADPH oxidase 1 and the production of reactive oxygen species in macrophages. Free Radical Biology and Medicine, 73 318-327. doi:10.1016/j.freeradbiomed.2014.05.020


Author Menon, Deepthi
Coll, Rebecca
O'Neill, Luke A. J.
Board, Philip G.
Title Glutathione transferase Omega 1 is required for the lipopolysaccharide- stimulated induction of NADPH oxidase 1 and the production of reactive oxygen species in macrophages
Journal name Free Radical Biology and Medicine   Check publisher's open access policy
ISSN 0891-5849
1873-4596
Publication date 2014-01-01
Year available 2014
Sub-type Article (original research)
DOI 10.1016/j.freeradbiomed.2014.05.020
Volume 73
Start page 318
End page 327
Total pages 10
Place of publication Philadelphia, PA United States
Publisher Elsevier
Collection year 2015
Language eng
Abstract Bacterial lipopolysaccharide (LPS) stimulation of macrophages and inflammation via the Toll-like receptor 4 (TLR4) signaling pathway through NF-κΒ generates reactive oxygen species (ROS) and proinflammatory cytokines such as IL-1β, IL-6, and TNFα. Because glutathione transferase Omega 1-1 (GSTO1-1) can catalyze redox reactions such as the deglutathionylation of proteins and has also been implicated in the release of IL-1β we investigated its role in the development of LPS-mediated inflammation. Our data show that shRNA knockdown of GSTO1-1 in macrophage-like J774.1A cells blocks the expression of NADPH oxidase 1 and the generation of ROS after LPS stimulation. Similar results were obtained with a GSTO1-1 inhibitor. To maintain high ROS levels during an inflammatory response, LPS stimulation causes the suppression of enzymes such as catalase and glutathione peroxidase that protect against oxidative stress. The knockdown of GSTO1-1 also attenuates this response. Our data indicate that GSTO1-1 needs to be catalytically active and mediates its effects on the LPS/TLR4 inflammatory pathway upstream of NF-κΒ. These data suggest that GSTO1-1 is a novel target for anti-inflammatory intervention.
Keyword Free radicals
Glutathione transferase Omega 1
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Non HERDC
Institute for Molecular Bioscience - Publications
 
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Created: Fri, 27 Mar 2015, 20:54:55 EST by Rebecca Coll on behalf of Institute for Molecular Bioscience