Vascular and Endovascular Surgery

 

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First published on March 4, 2008, doi:10.1177/1538574408314440

Vascular and Endovascular Surgery 2008;42:256.

A more recent version of this article appeared on June 1, 2008

Article

Thrombospondin-1-Induced Migration Is Functionally Dependent Upon Focal Adhesion Kinase

Xiu-Jie Wang, Kristopher G. Maier, Shoichi Fuse, Alliric Willis, Susan Nesselroth, Bauer Sumpio, and Vivian Gahtan*

* To whom correspondence should be addressed. E-mail: gahtanv{at}upstate.edu.


  Abstract
Vascular smooth muscle cell migration is important in vascular disease. Previously, we showed thrombospondin-1 activates focal adhesion kinase in these cells. We hypothesized that focal adhesion kinase is important for thrombspondin-1-induced vascular smooth muscle cell migration. Bovine aortic smooth muscle cells were transfected with FAK397, FAK-wild type, pcDNA, or {beta}-Gal plasmids. Migration was assessed with thrombospondin-1 or serum-free medium in quiescent transfected cells or quiescent cells pretreated with the focal adhesion kinase inhibitor, geldanamycin. Number of cells migrated per 5 fields (x400) were recorded. Antihemagglutinin immunoprecipitation and Western blot were used to examine thrombospondin-1induced focal adhesion kinase phosphorylation in transfected cells. FAK397 transfection inhibited thrombospondin-1-induced focal adhesion kinase phosphorylation and migration (P<.05). Geldanamycin inhibited thrombospondin-1-induced smooth muscle cell migration (P<.05). In conclusion, vascular smooth muscle cells transfected with FAK397 inhibited thrombosponin1-induced migration and tyrosine phosphorylation. Further, geldanamycin also inhibited migration. These results suggest focal adhesion kinase is involved in thrombospondin-1-induced vascular smooth muscle cell migration.


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