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Am J Physiol Cell Physiol 297: C814-C822, 2009. First published July 8, 2009; doi:10.1152/ajpcell.00226.2009
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VASCULAR BIOLOGY

Focal adhesion kinase modulates activation of NF-{kappa}B by flow in endothelial cells

Tobias Petzold,1,2 A. Wayne Orr,1,2 Cornelia Hahn,1,2 Krishna A. Jhaveri,1,2 J. Thomas Parsons,2 and Martin Alexander Schwartz1,2,3

1Robert M. Berne Cardiovascular Research Center, 2Department of Microbiology, and 3Department of Biomedical Engineering, University of Virginia, Charlottesville, Virginia

Submitted 22 May 2009 ; accepted in final form 30 June 2009

Atherogenesis involves activation of NF-{kappa}B in endothelial cells by fluid shear stress. Because this pathway involves integrins, we investigated the involvement of focal adhesion kinase (FAK). We found that FAK was not required for flow-stimulated translocation of the p65 NF-{kappa}B subunit to the nucleus but was essential for phosphorylation of p65 on serine 536 and induction of ICAM-1, an NF-{kappa}B-dependent gene. NF-{kappa}B activation by TNF-{alpha} or hydrogen peroxide was FAK independent. Events upstream of NF-{kappa}B, including integrin activation, Rac activation, reactive oxygen production, and degradation of I{kappa}B, were FAK independent. FAK therefore regulates NF-{kappa}B phosphorylation and transcriptional activity in response to flow by a novel mechanism.

atherosclerosis; fluid shear stress; integrin signaling; mechanotransduction


Address for reprint requests and other correspondence: M. Schwartz, Dept. of Microbiology, Univ. of Virginia, Charlottesville, VA 22908 (e-mail: maschwartz{at}virginia.edu).




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S. Chien, J.-J. Chiu, and Y.-S. Li
Focal adhesion kinase phosphorylation in flow-activation of endothelial NF-{kappa}B. Focus on "Focal adhesion kinase modulates activation of NF-{kappa}B by flow in endothelial cells"
Am J Physiol Cell Physiol, October 1, 2009; 297(4): C800 - C801.
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