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Biochem Biophys Res Commun. 1998 Jul 30;248(3):635-40.

Endothelial cell spreading on type IV collagen and spreading-induced FAK phosphorylation is regulated by Ca2+ influx.

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Molecular Signaling Section, National Cancer Institute, Bethesda, Maryland 20892, USA.


The interaction of endothelial cells with their basement membrane and local stroma is highly regulated. The observation that CAI, an inhibitor of Ca++ influx, inhibited human umbilical vein endothelial cell (HUVEC) adhesion suggested that Ca++ influx was a regulator of HUVEC-matrix interaction. Exposure of HUVEC cells to CAI or SK&F 96365, another Ca++ influx inhibitor, selectively blocked spreading but not attachment on type IV collagen but not type I collagen. Ca++ influx blockade also prevented spreading-induced FAK phosphorylation and kinase activity and secondary paxillin phosphorylation. No inhibitory effect was observed when the cells spread on type I collagen. The inhibitory effect of CAI on spreading and spreading-associated FAK phosphorylation and kinase activity was reversible. These data indicate that HUVEC cells have a selective requirement for Ca++ influx for spreading and downstream signaling on basement membrane type IV collagen.

[Indexed for MEDLINE]

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