 exposure of low - passage endothelial cells in culture to nonlethal amounts of asbestos , but not refractory ceramic fiber-1 , increases cell motility and gene expression . 
 these changes may be initiated by the fibers mimicking matrix proteins as ligands for receptors on the cell surface . in the present study , 1- to 3-hr exposures of endothelial cells to 5 
 mg / cm2 of chrysotile asbestos caused marked cell elongation and motility . 
 however , little morphological change was seen when chrysotile was added to cells pretreated with either mannosamine to prevent assembly of glycophosphatidylinositol ( gpi)-anchored receptors or with herbimycin a to inhibit tyrosine kinase activity . 
 affinity purification of gpi - anchored urokinase - type plasminogen activator receptor ( upar ) from chrysotile - exposed cells demonstrated that asbestos altered the profile of proteins and phosphoproteins complexed with this receptor . 
 tyrosine kinase activities in the complexes were also increased by asbestos . 
 immunoprecipitations with selective monoclonal antibodies demonstrated that both chrysotile and crocidolite asbestos increase kinase activities associated with p60 src or p120 focal adhesion kinase ( fak ) . 
 further , chrysotile also changed the profile of proteins and phosphoproteins associated with fak in intact cells . 
 these data suggest that asbestos initiates endothelial cell phenotypic change through interactions with upar - containing complexes and that this change is mediated through tyrosine kinase cascades.imagesfigure 1 . 
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