The role of focal adhesion kinase in vascular smooth muscle cell migration Public Deposited

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Last Modified
  • March 21, 2019
Creator
  • Mangiante, Lee Elena
    • Affiliation: School of Medicine, Department of Pathology and Laboratory Medicine
Abstract
  • Focal adhesion kinase (FAK) integrates diverse signaling pathways to regulate proliferation, migration, and differentiation. Germline deletion of FAK in mice results in embryonic lethality with pronounced defects in vascular structure and integrity, implicating FAK as critical to the development and migration of vascular smooth muscle cells (SMCs). However, the precise function of FAK in SMCs remains elusive. Primary aortic SMCs from fakflox/flox mice were infected with Cre-expressing adenovirus, ablating FAK production. FAK deletion inhibited migration to platelet-derived growth factor (PDGF). While PDGF-induced membrane ruffling was FAK-independent, PDGF-induced polarization was reduced fivefold in FAK-depleted cells. The RhoA effector, Dia2, localized to focal adhesions in a FAK-dependent manner, and ablation of FAK attenuated myosin light chain phosphorylation. Finally, we detected a novel interaction between Dia2 and the Arp2/3 activator, cortactin. These data suggest that FAK may promote cell contraction and polarized migration toward PDGF by regulating distinct pools of RhoA activity.
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  • In Copyright
Advisor
  • Taylor, Joan
Degree granting institution
  • University of North Carolina at Chapel Hill
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  • Open access
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