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Articles in PresS, published online ahead of print June 26, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.00064.2002
Submitted on February 12, 2002
Accepted on June 19, 2002
vß3 Integrin in TNF-Induced Endothelial Cell Migration
1 Department of Physiology, Albany Medical College, Albany, NY, USA; Center for Cell Biology & Cancer Research, Albany Medical College, Albany, NY, USA; Laboratory of Cell Physiology, Veterans Affairs Medical Center, Washington, DC, USA
2 Department of Physiology, Albany Medical College, Albany, NY, USA; Center for Cell Biology & Cancer Research, Albany Medical College, Albany, NY, USA
3 Laboratory of Cell Physiology, Veterans Affairs Medical Center, Washington, DC, USA
* To whom correspondence should be addressed. E-mail: baochong.gao{at}med.va.gov.
Tumor necrosis factor (TNF), one of the major inflammatory cytokines, is known to influence endothelial cell migration. In this study, we demonstrated that exposure of calf pulmonary artery endothelial cells to TNF caused an increase in the formation of membrane protrusions and cell migration. Fluorescence microscopy revealed an increase in vß3 focal contacts, but a decrease in 5ß1 focal contacts in TNF-treated cells. In addition, both cell-surface and total cellular expression of vß3 integrins increased significantly, whereas the expression of 5ß1 integrins was unaltered. Only focal contacts containing vß3, but not 5ß1, integrins were present in membrane protrusions of cells at the migration front. In contrast, robust focal contacts containing 5ß1 integrins were present in cells behind the migration front. A blocking antibody to vß3, but not a blocking antibody to 5 integrins, significantly inhibited TNF-induced cell migration. These results indicate that in response to TNF, endothelial cells may increase the activation and ligation of vß3 while decrease the activation and ligation of 5ß1 integrins to facilitate cell migration, a process essential for vascular wound healing and angiogenesis.
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