IRS-2 deficiency in macrophages promotes their accumulation in the vascular wall

Biochem Biophys Res Commun. 2011 Dec 2;415(4):545-50. doi: 10.1016/j.bbrc.2011.10.086. Epub 2011 Nov 2.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blood Vessels / immunology*
  • Bone Marrow Transplantation
  • Chemokine CCL2 / metabolism
  • Insulin Receptor Substrate Proteins / deficiency*
  • Insulin Receptor Substrate Proteins / genetics
  • Macrophages / immunology*
  • Mice
  • Mice, Inbred C57BL

Substances

  • Ccl2 protein, mouse
  • Chemokine CCL2
  • Insulin Receptor Substrate Proteins
  • Irs2 protein, mouse