Abstract
Although potential contribution of endothelial progenitor cells (EPCs) to angiogenesis in glioma has been proposed, the molecular mechanisms of EPCs recruitment to vasculature have not been fully elucidated. Here, we show that the supernatant from glioma cells promotes EPCs angiogenesis via VEGFR-2, not VEGFR-1. Moreover, VEGFR-2 siRNA inhibits VEGFR-2 expression in EPCs, tube formation on matrigel and cell migration. MMP-9 activity and expression and the Akt and ERK phosphorylations are decreased by VEGFR-2 siRNA. Thus, these results indicate that glioma cells enhance EPC angiogenesis via VEGFR-2, not VEGFR-1, mediated by the MMP-9, Akt and ERK signal pathways.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Brain Neoplasms / metabolism*
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Cell Line, Tumor
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Endothelial Cells / cytology*
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Extracellular Signal-Regulated MAP Kinases / metabolism
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Gene Expression Regulation, Neoplastic*
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Glioma / metabolism*
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Humans
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Matrix Metalloproteinase 9 / metabolism
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Models, Biological
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Neovascularization, Pathologic*
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Phosphorylation
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Proto-Oncogene Proteins c-akt / metabolism
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Stem Cells / metabolism
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Vascular Endothelial Growth Factor Receptor-1 / metabolism*
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Vascular Endothelial Growth Factor Receptor-2 / metabolism*
Substances
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Vascular Endothelial Growth Factor Receptor-1
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Vascular Endothelial Growth Factor Receptor-2
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Proto-Oncogene Proteins c-akt
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Extracellular Signal-Regulated MAP Kinases
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Matrix Metalloproteinase 9