Exp Mol Med.  2006 Apr;38(2):153-161.

betaig-h3 triggers signaling pathways mediating adhesion and migration of vascular smooth muscle cells through alphavbeta5 integrin

Affiliations
  • 1Department of Biochemistry and Cell and Matrix Biology Research Institute, School of Medicine, Kyungpook National University, Daegu 700-422, Korea. iskim@mail.knu.ac.kr
  • 2Department of Molecular Medicine, School of Medicine, Kyungpook National University, Daegu 700-422, Korea.
  • 3Department of Internal Medicine, School of Medicine, Kyungpook National University, Daegu 700-422, Korea.

Abstract

Adhesion and migration of vascular smooth muscle cells (VSMCs) play an important role in the pathogenesis of atherosclerosis. These processes involve the interaction of VSMCs with extracellular matrix proteins. Here, we investigated integrin isoforms and signaling pathways mediating the adhesion and migration of VSMCs on betaig-h3, a transforming growth factor (TGF)-beta-inducible extracellular matrix protein that is elevated in atherosclerotic plaques. Adhesion assays showed that the alphavbeta5 integrin is a functional receptor for the adhesion of aortic VSMCs to betaig-h3. An YH18 motif containing amino acids between 563 and 580 of betaig-h3 was an essential motif for the adhesion and growth of VSMCs. Interaction between the YH18 motif and the alphavbeta5 integrin was responsible for the migration of VSMCs on betaig-h3. Inhibitors of phosphatidylinositide 3-kinase, extracellular signal-regulated kinase (ERK), and Src kinase reduced the adhesion and migration of VSMCs on betaig-h3. betaig-h3 triggered phosphorylation and activation of AKT, ERK, focal adhesion kinase, and paxillin mediating the adhesion and migration of VSMCs. Taken together, these results suggest that betaig-h3 and alphavbeta5 integrin play a role in the adhesion and migration of VSMCs during the pathogenesis of atherosclerosis.

Keyword

atherosclerosis; betaIG-H3 protein; integrin alpahvbeta5; muscle; smooth; vascular; transforming growth factor beta
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