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Am J Physiol Lung Cell Mol Physiol (January 4, 2002). doi:10.1152/ajplung.00174.2001
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Articles in PresS, published online ahead of print January 4, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00174.2001
Submitted on May 23, 2001
Accepted on December 14, 2001

FAK Blunts Adenosine/Homocysteine-Induced Endothelial Cell Apoptosis: Requirement for PI 3-kinase

Robert E Bellas, Elizabeth O Harrington, Kerri L Sheahan, Julie Newton, Caroline Marcus, and Sharon Rounds*

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

Treatment of cultured bovine pulmonary endothelial cells (BPAEC) with adenosine (Ado) alone, or in combination with homocysteine (Hc), leads to disruption of focal adhesion complexes, caspase-dependent degradation of components of focal adhesions and subsequent apoptosis. Endothelial cells transiently overexpressing paxillin or p130Cas cDNAs underwent Ado/Hc-induced apoptosis to a similar extent compared to cells transfected with vector alone. However, overexpression of focal adhesion kinase (FAK) cDNA blunted Ado/Hc-induced apoptosis. FAK constructs lacking the central catalytic domain or containing a point mutation, rendering the catalytic domain enzymatically inactive, did not provide protection from apoptosis. Constructs containing a mutation in the major autophosphorylation site (tyrosine 397) similarly did not prevent cell death. A FAK mutant in amino acid 395, deficient in phosphatidylinositol 3-kinase (PI 3-kinase) binding, was not able to blunt apoptosis. Finally, overexpression of FAK did not provide protection from apoptosis in the presence of LY294002, a PI 3-kinase inhibitor. Taken together, these data suggest that the survival signals mediated by overexpression of FAK in response to Ado/Hc-induced apoptosis require PI 3-kinase-dependent pathway.




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