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IRS-2 deficiency in macrophages promotes their accumulation in the vascular wall.
MedLine Citation:
PMID:  22074825     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
The aim of this study was to investigate the role of insulin receptor substrate-2 (IRS-2) mediated signal in macrophages on the accumulation of macrophages in the vascular wall. Mice transplanted with IRS-2(-/-) bone marrow, a model of myeloid cell restricted defect of IRS-2, showed accumulation of monocyte chemoattractant protein-1-expressing macrophages in the vascular wall. Experiments using cultured peritoneal macrophages showed that IRS-2-mediated signal pathway stimulated by physiological concentrations of insulin, not by IL-4, contributed to the suppression of monocyte chemoattractant protein-1 expression induced by lipopolysaccharide. Our data indicated that IRS-2 deficiency in macrophages enhanced their accumulation in the vascular wall accompanied by increased expression of proinflammatory mediators in macrophages. These results suggest a role for insulin resistance in macrophages in early atherosclerogenesis.
Authors:
Tomoya Mita; Kosuke Azuma; Hiromasa Goto; Wen Long Jin; Masayuki Arakawa; Takashi Nomiyama; Ryo Suzuki; Naoto Kubota; Kazuyuki Tobe; Takashi Kadowaki; Yoshio Fujitani; Takahisa Hirose; Ryuzo Kawamori; Hirotaka Watada
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2011-11-2
Journal Detail:
Title:  Biochemical and biophysical research communications     Volume:  -     ISSN:  1090-2104     ISO Abbreviation:  -     Publication Date:  2011 Nov 
Date Detail:
Created Date:  2011-11-14     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0372516     Medline TA:  Biochem Biophys Res Commun     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2011 Elsevier Inc. All rights reserved.
Affiliation:
Department of Medicine, Metabolism and Endocrinology, Juntendo University Graduate School of Medicine, Tokyo 113-8421, Japan.
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