Abstract
A number of factors both stimulating and inhibiting angiogenesis have been described. In the current work, we demonstrate that the angiogenic factor vascular endothelial growth factor (VEGF) activates mitogen-activated protein kinase (MAPK) as has been previously shown for basic fibroblast growth factor. The antiagiogenic factor 16-kDa N-terminal fragment of human prolactin inhibits activation of MAPK distal to autophosphorylation of the putative VEGF receptor, Flk-1, and phospholipase C-gamma. These data show that activation and inhibition of MAPK may play a central role in the control of angiogenesis.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Blotting, Western
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Calcium-Calmodulin-Dependent Protein Kinases / metabolism*
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Capillaries
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Cattle
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Cells, Cultured
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Cerebrovascular Circulation
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Electrophoresis, Polyacrylamide Gel
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Endothelial Growth Factors / pharmacology*
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Endothelium, Vascular / enzymology*
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Enzyme Activation
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Fibroblast Growth Factor 2 / pharmacology*
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Humans
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Lymphokines / pharmacology*
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Molecular Weight
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Peptide Fragments / pharmacology*
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Phosphoproteins / isolation & purification
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Phosphoproteins / metabolism
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Phosphotyrosine
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Prolactin / pharmacology*
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Recombinant Proteins / pharmacology
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Tyrosine / analogs & derivatives
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Tyrosine / analysis
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Vascular Endothelial Growth Factor A
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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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Phosphoproteins
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Recombinant Proteins
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Vascular Endothelial Growth Factor A
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Vascular Endothelial Growth Factors
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Fibroblast Growth Factor 2
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Phosphotyrosine
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Tyrosine
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Prolactin
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Calcium-Calmodulin-Dependent Protein Kinases