VLA-2 MEDIATES THE INTERACTION OF COLLAGEN WITH ENDOTHELIUM DURING IN-VITRO VASCULAR TUBE FORMATION

被引:23
作者
JACKSON, CJ
KNOP, A
GILES, I
JENKINS, K
SCHRIEBER, L
机构
[1] Department of Medicine, University of Sydney, Sutton Rheumatism Research Laboratory, St Leonards
关键词
D O I
10.1006/cbir.1994.1122
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
A confluent endothelial monolayer can be induced to form vascular tubes in response to collagen. We investigated possible mechanisms of collagen-induced tube formation by using antibodies to the VLA-2 integrin receptor and protein kinase C inhibitors. Pre-incubation of cells with anti-VLA-2 (which recognises both the alpha(2) and beta(1) chains) and AK7 (which recognises only the alpha(2) chain) showed a dose-dependent inhibition of tube formation. At 50 mu g/ml, anti-VLA-2 completely inhibited collagen-induced tube formation, whereas AK7 caused only partial inhibition. Both chlorpromazine and trifluoperazine, at concentrations of 1O mu M, prevented tube formation (> 40% inhibition). In summary, the VLA-2 integrin receptor plays a role in the induction of tube formation by type I collagen. Protein kinase C may be activated during this process.
引用
收藏
页码:859 / 867
页数:9
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