| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2899490 | Cardiovascular Pathology | 2007 | 9 Pages |
IntroductionConstrictive remodeling of the neointima results in the late lumen loss and restenosis after balloon angioplasty. Intense expression of α8β1 integrin in the contractile state of vascular smooth muscle cells (VSMCs) and in myofibroblasts led us to hypothesize that it might be involved in the process of late constrictive remodeling.Methods and resultsBalloon injury was used to induce neointima formation in the rat carotid artery. Immunohistochemical analysis and immunoconfocal studies showed that late lumen narrowing was concomitant with the up-regulation of smooth muscle α-actin and α8 integrin in the neointima. The transforming growth factor-beta (TGF-β)-induced contractile properties of fibroblasts and VSMCs populated in a three-dimensional collagen matrix was associated with up-regulation of α8 integrin. TGF-β-induced myofibroblastic features in Rat1 fibroblasts were impaired in cells pretreated with a small interference RNA silencing the α8 integrin gene.ConclusionThe close correlation between α8 integrin up-regulation in the neointima and late luminal loss and α8 integrin being required for contractile properties induced by TGF-β highlight a possible role for α8 integrin in postangioplasty restenosis.
