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VLA‐2 mediates the interaction of collagen with endothelium during in vitro vascular tube formation.
Author(s) -
Jackson Christopher J.,
Knop Alison,
Giles Irina,
Jenkins Kate,
Schrieber Les
Publication year - 1994
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1006/cbir.1994.1122
Subject(s) - in vitro , integrin , trifluoperazine , chemistry , receptor , microbiology and biotechnology , incubation , type i collagen , biophysics , biochemistry , endocrinology , biology , enzyme , calmodulin
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 α2 and β1 chains) and AK7 (which recognises only the α2 chain) showed a dose‐dependent inhibition of tube formation. At 50 μg/ml, anti‐VLA‐2 completely inhibited collagen‐induced tube formation, whereas AK7 caused only partial inhibition. Both chlorpromazine and trifluoperazine, at concentrations of 10μM, 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.