Online Archive of University of Virginia Scholarship
The Role of Focal Adhesion Kinase in Flow Induced Signaling889 views
Author
Petzold, Tobias, Department of Microbiology, University of Virginia
Advisors
Parsons, Thomas, Department of Microbiology, University of Virginia
Abstract
Atherosclerosis is a chronic vascular inflammatory disease that develops in areas of disturbed flow like artery bifurcations and branch points. The transcription factor NF-kB is activated in atherosclerotic lesions and stimulates E-selectin, ICAM-1 and VCAM-1 expression, which mediate leukocyte recruitment. NF-kB activation by flow is downstream of integrin activation. Focal adhesion kinase (FAK) is a critical mediator of integrin signaling. To test FAK's role in flowinduced NF-kB activation, I isolated mouse aortic endothelial cells from conditional FAK knockout mice. Cre adenovirus caused complete loss of FAK from the conditional cells. Shear stress activated NF-kB in WT but not FAK-/- endothelial cells, whereas Erk activation was similar in both cell types. While, reactive oxygen species (ROS) are critical mediators of flow induced NF-kB activation production their production was unaffected in FAK-/- cells, arguing the FAK might be involved in a distinct pathway of NF-kB activation by flow.
Note: Abstract extracted from PDF text
Petzold, Tobias. The Role of Focal Adhesion Kinase in Flow Induced Signaling. University of Virginia, Department of Microbiology, MA (Master of Arts), 2007-01-01, https://doi.org/10.18130/V32T1K.
