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Department of Bioengineering and Whitaker Institute of Biomedical Engineering, University of California at San Diego, La Jolla, California 92093
Blood flow can modulate vascular cell
functions. We studied interactions between integrins and Flk-1 in
transducing the mechanical shear stress due to flow. This application
of a step shear stress caused Flk-1 · Casitas B-lineage
lymphoma (Cbl) activation (Flk-1 · Cbl association, tyrosine
phosphorylation of the Cbl-bound Flk-1, and tyrosine phosphorylation of
Cbl) in bovine aortic endothelial cells (BAECs). The activation of
integrins by plating BAECs on vitronectin or fibronectin also induced
this Flk-1 · Cbl activation. The shear-induced
Flk-1 · Cbl activation was blocked by inhibitory antibodies for
v
3- or 1-integrin,
suggesting that it is mediated by integrins. Inhibition of Flk-1 by
SU1498 also abolished this shear-induced Flk-1 · Cbl
activation. In contrast to the requirement of integrins for
Flk-1 · Cbl activation, the Flk-1 blocker SU1498 had no
detectable effect on the shear-induced integrin activation, suggesting
that integrins and Flk-1 play sequential roles in the signal
transduction hierarchy induced by shear stress. Integrins are essential
for the mechanical activation of Flk-1 by shear stress but not for the
chemical activation of Flk-1 by VEGF.
mechanotransduction; vascular endothelial growth factor; Casitas B-lineage lymphoma
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