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Publication : PECAM-1 is necessary for flow-induced vascular remodeling.

First Author  Chen Z Year  2009
Journal  Arterioscler Thromb Vasc Biol Volume  29
Issue  7 Pages  1067-73
PubMed ID  19390054 Mgi Jnum  J:167818
Mgi Id  MGI:4880637 Doi  10.1161/ATVBAHA.109.186692
Citation  Chen Z, et al. (2009) PECAM-1 is necessary for flow-induced vascular remodeling. Arterioscler Thromb Vasc Biol 29(7):1067-73
abstractText  OBJECTIVE: Vascular remodeling is a physiological process that occurs in response to long-term changes in hemodynamic conditions, but may also contribute to the pathophysiology of intima-media thickening (IMT) and vascular disease. Shear stress detection by the endothelium is thought to be an important determinant of vascular remodeling. Previous work showed that platelet endothelial cell adhesion molecule-1 (PECAM-1) is a component of a mechanosensory complex that mediates endothelial cell (EC) responses to shear stress. METHODS AND RESULTS: We tested the hypothesis that PECAM-1 contributes to vascular remodeling by analyzing the response to partial carotid artery ligation in PECAM-1 knockout mice and wild-type littermates. PECAM-1 deficiency resulted in impaired vascular remodeling and significantly reduced IMT in areas of low flow. Inward remodeling was associated with PECAM-1-dependent NFkappaB activation, surface adhesion molecule expression, and leukocyte infiltration as well as Akt activation and vascular cell proliferation. CONCLUSIONS: PECAM-1 plays a crucial role in the activation of the NFkappaB and Akt pathways and inflammatory cell accumulation during vascular remodeling and IMT. Elucidation of some of the signals that drive vascular remodeling represent pharmacologically tractable targets for the treatment of restenosis after balloon angioplasty or stent placement.
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