Publication | Open Access
Angiostatin induces endothelial cell apoptosis and activation of focal adhesion kinase independently of the integrin-binding motif RGD
347
Citations
21
References
1998
Year
Adhesion Plaque FormationCell AdhesionImmunologyCell DeathPathologyInflammationAngiogenesisIntegrin-binding Motif RgdFibroblast Growth FactorAngiostatin TreatmentMatrix BiologyFocal Adhesion KinaseAtherosclerosisCell SignalingVascular BiologyNeovascularizationVascular Endothelial Growth FactorSclerodermaPharmacologyCell BiologyTumor MicroenvironmentEndothelial DysfunctionCell-matrix InteractionEndothelial Cell ApoptosisMedicineExtracellular Matrix
Angiostatin, a fragment of plasminogen, has been identified and characterized as an endogenous inhibitor of neovascularization. We show that angiostatin treatment of endothelial cells in the absence of growth factors results in an increased apoptotic index whereas the proliferation index is unchanged. Angiostatin also inhibits migration and tube formation of endothelial cells. Angiostatin treatment has no effect on growth factor-induced signal transduction but leads to an RGD-independent induction of the kinase activity of focal adhesion kinase, suggesting that the biological effects of angiostatin relate to subversion of adhesion plaque formation in endothelial cells.
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