Abstract
Platelets secrete platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) upon stimulation. We have demonstrated that platelets have functionally active PDGF alpha-receptors, a transmembrane tyrosine kinase involved in negative feedback regulation. Here we demonstrate the presence of the related VEGF receptors fms-like tyrosine kinase-1 and kinase-insert domain region on human platelets. VEGF itself did not cause platelet aggregation. However, addition of exogenous VEGF to SFRLLN or thrombin-stimulated platelets potentiated platelet aggregation. Moreover, thrombin-induced phosphoinositide 3-kinase and mitogen-activated protein kinase activity were enhanced in the presence of VEGF.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Blood Platelets / drug effects*
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Endothelial Growth Factors / pharmacology*
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Humans
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Lymphokines / pharmacology*
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Mitogen-Activated Protein Kinases / metabolism
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Peptide Fragments / pharmacology
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Phosphatidylinositol 3-Kinases / metabolism
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Platelet Activation
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Proto-Oncogene Proteins / isolation & purification*
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Receptor Protein-Tyrosine Kinases / isolation & purification*
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Receptors, Growth Factor / isolation & purification*
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Receptors, Thrombin / metabolism
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Receptors, Vascular Endothelial Growth Factor
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Signal Transduction
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Thrombin / pharmacology
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Vascular Endothelial Growth Factor A
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Vascular Endothelial Growth Factor Receptor-1
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Vascular Endothelial Growth Factors
Substances
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Endothelial Growth Factors
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Lymphokines
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Peptide Fragments
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Proto-Oncogene Proteins
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Receptors, Growth Factor
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Receptors, Thrombin
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Vascular Endothelial Growth Factor A
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Vascular Endothelial Growth Factors
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thrombin receptor peptide (42-47)
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Phosphatidylinositol 3-Kinases
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Receptor Protein-Tyrosine Kinases
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Receptors, Vascular Endothelial Growth Factor
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Vascular Endothelial Growth Factor Receptor-1
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Mitogen-Activated Protein Kinases
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Thrombin