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VASCULAR BIOLOGY

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

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-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-B subunit to the nucleus but was essential for phosphorylation of p65 on serine 536 and induction of ICAM-1, an NF-B-dependent gene. NF-B activation by TNF- or hydrogen peroxide was FAK independent. Events upstream of NF-B, including integrin activation, Rac activation, reactive oxygen production, and degradation of IB, were FAK independent. FAK therefore regulates NF-B phosphorylation and transcriptional activity in response to flow by a novel mechanism.

atherosclerosis; fluid shear stress; integrin signaling; mechanotransduction

This article has been cited by other articles:

				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. [Full Text] [PDF]