Alessandro R, Masiero L, Lapidos K, Spoonster J, Kohn E C
Molecular Signaling Section, National Cancer Institute, Bethesda, Maryland 20892, USA.
Biochem Biophys Res Commun. 1998 Jul 30;248(3):635-40. doi: 10.1006/bbrc.1998.8705.
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.
内皮细胞与其基底膜和局部基质之间的相互作用受到高度调控。钙内流抑制剂CAI抑制人脐静脉内皮细胞（HUVEC）黏附这一观察结果表明，钙内流是HUVEC与基质相互作用的调节因子。将HUVEC细胞暴露于CAI或另一种钙内流抑制剂SK&F 96365，可选择性地阻断其在IV型胶原而非I型胶原上的铺展，但不影响其黏附。钙内流阻断还可防止铺展诱导的黏着斑激酶（FAK）磷酸化和激酶活性以及继发性桩蛋白磷酸化。当细胞在I型胶原上铺展时未观察到抑制作用。CAI对铺展以及与铺展相关的FAK磷酸化和激酶活性的抑制作用是可逆的。这些数据表明，HUVEC细胞在基底膜IV型胶原上进行铺展和下游信号传导时对钙内流有选择性需求。
