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

Section of Vascular Surgery, Yale University School of Medicine, New Haven

Kristopher Maier

Connecticut, Division of Vascular Surgery and Endovascular Services, SUNY Upstate Medical University, Department of Veterans Affairs, VA Healthcare Network Upstate New York Syracuse, New York

Shoichi Fuse, MD

Section of Vascular Surgery, Yale University School of Medicine, New Haven

Alliric I. Willis, MD

Section of Vascular Surgery, Yale University School of Medicine, New Haven

Eric Olson

Section of Vascular Surgery, Yale University School of Medicine, New Haven

Susan Nesselroth, MD

Section of Vascular Surgery, Yale University School of Medicine, New Haven

Bauer E. Sumpio, MD

Section of Vascular Surgery, Yale University School of Medicine, New Haven, The VA Connecticut Health Care System, West Haven

Vivian Gahtan, MD

Section of Vascular Surgery, Yale University School of Medicine, New Haven, gahtanv{at}upstate.edu, The VA Connecticut Health Care System, West Haven, Department of Veterans Affairs, VA Healthcare Network Upstate New York Syracuse, New York

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 β-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-1-induced 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 thrombosponin-1-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.

Key Words: thrombospondin-1 • migration • chemotaxis • focal adhesion kinase • geldanamycin • smooth muscle cell

This version was published on June 1, 2008

Vascular and Endovascular Surgery, Vol. 42, No. 3, 256-262 (2008)
DOI: 10.1177/1538574408314440


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