title: [Transforming growth factor beta and fibroblast growth factor have opposite effects on the proliferation of endothelial cells].
abstract: Recent data indicate that beta type transforming growth factor (TGF-beta) may be a bifunctional regulator of cellular growth: it induces anchorage-independent growth of certain cells but is also capable of inhibiting anchorage-dependent or -independent proliferation of a variety of normal epithelial and transformed cells. We show that TGF-beta is also a reversible inhibitor of proliferation of bovine aortic endothelial cells in culture. TGF-beta inhibits the proliferation of endothelial cells grown in the presence of basic fibroblast growth factor (bFGF). Dose-dependent inhibition occurs at 0.2-2.0 ng/ml TGF-beta. Inhibition of cell proliferation in the presence of a maximally stimulating dose of bFGF is not overcome by a tenfold excess of bFGF, suggesting that antagonism of bFGF-induced cell proliferation by TGF-beta is of a non-competitive nature. TGF-beta affects the morphology of confluent cells in a reversible manner.
authors.forename: M
authors.initials: M
authors.lastname: Fràter-Schröder
authors.forename: G
authors.initials: G
authors.lastname: Müller
authors.forename: W
authors.initials: W
authors.lastname: Birchmeier
authors.forename: P
authors.initials: P
authors.lastname: Böhlen
mesh_terms: D000818:Animals; D002417:Cattle; D002455:Cell Division / Q000187:drug effects*; D002478:Cells, Cultured; D004727:Endothelium / Q000166:cytology; D005346:Fibroblast Growth Factors / Q000037:antagonists & inhibitors* / Q000494:pharmacology; D006131:Growth Inhibitors; D006133:Growth Substances / Q000494:pharmacology; D006801:Humans; D010455:Peptides / Q000037:antagonists & inhibitors* / Q000494:pharmacology; D015291:Transforming Growth Factors
chemical_list: D006131:Growth Inhibitors; D006133:Growth Substances; D010455:Peptides; D005346:Fibroblast Growth Factors; D015291:Transforming Growth Factors
vernacular_title: Transforming growth factor-beta und fibroblast growth factor wirken entgegengesetzt auf die Proliferation von Endothelzellen.