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Am J Physiol Cell Physiol 283: C1196-C1205, 2002. First published June 26, 2002; doi:10.1152/ajpcell.00064.2002
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Vol. 283, Issue 4, C1196-C1205, October 2002

Role of alpha vbeta 3-integrin in TNF-alpha -induced endothelial cell migration

Baochong Gao1,2,3, Thomas M. Saba1,2, and Min-Fu Tsan3

1 Department of Physiology and 2 Center for Cell Biology and Cancer Research, Albany Medical College, Albany, New York 12208, and 3 Laboratory of Cell Physiology, Veterans Affairs Medical Center, Washington, District of Columbia 20422

Tumor necrosis factor-alpha (TNF-alpha ), one of the major inflammatory cytokines, is known to influence endothelial cell migration. In this study, we demonstrate that exposure of calf pulmonary artery endothelial cells to TNF-alpha caused an increase in the formation of membrane protrusions and cell migration. Fluorescence microscopy revealed an increase in alpha vbeta 3 focal contacts but a decrease in alpha 5beta 1 focal contacts in TNF-alpha -treated cells. In addition, both cell-surface and total cellular expression of alpha vbeta 3-integrins increased significantly, whereas the expression of alpha 5beta 1-integrins was unaltered. Only focal contacts containing alpha vbeta 3- but not alpha 5beta 1-integrins were present in membrane protrusions of cells at the migration front. In contrast, robust focal contacts containing alpha 5beta 1-integrins were present in cells behind the migration front. A blocking antibody to alpha vbeta 3, but not a blocking antibody to alpha 5-integrins, significantly inhibited TNF-alpha -induced cell migration. These results indicate that in response to TNF-alpha , endothelial cells may increase the activation and ligation of alpha vbeta 3 while decreasing the activation and ligation of alpha 5beta 1-integrins to facilitate cell migration, a process essential for vascular wound healing and angiogenesis.

integrins; focal contacts; tumor necrosis factor-alpha


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