Abstract
The vascular endothelial growth factor (VEGF)-related factor, placental growth factor (PlGF),has been shown recently to play an important role in pathological VEGF-driven angiogenesis. In this study, we examine the effects of mPlGF/PlGF-2 overexpression in tumors grown from glioma cells containing a tetracycline-regulated mPlGF cDNA. Overexpression of mPlGF leads to increased tumor growth and vascular survival. When tetracycline is used to abruptly withdraw mPlGF overexpression, we see increased apoptosis in both vascular cells and macrophages. In addition, PlGF-2 induces survival gene expression and inhibits apoptosis in vitro. Thus, we propose that PlGF-2 contributes to tumor angiogenesis by providing increased survival function to endothelial cells and macrophages.
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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Cattle
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Cell Survival / physiology
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Chromosomal Proteins, Non-Histone / biosynthesis
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Chromosomal Proteins, Non-Histone / genetics
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Endothelium, Vascular / cytology*
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Endothelium, Vascular / metabolism
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Endothelium, Vascular / physiology
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Glioma / blood supply*
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Glioma / genetics
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Glioma / metabolism
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Glioma / pathology
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Humans
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Inhibitor of Apoptosis Proteins
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Macrophages / cytology*
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Macrophages / metabolism
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Macrophages / physiology
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Mice
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Mice, Nude
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Microtubule-Associated Proteins*
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Neoplasm Proteins
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Placenta Growth Factor
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Pregnancy Proteins / biosynthesis
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Pregnancy Proteins / genetics
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Pregnancy Proteins / physiology*
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Rats
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Survivin
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Up-Regulation
Substances
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BIRC5 protein, human
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Chromosomal Proteins, Non-Histone
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Inhibitor of Apoptosis Proteins
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Microtubule-Associated Proteins
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Neoplasm Proteins
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PGF protein, human
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Pgf protein, mouse
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Pgf protein, rat
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Pregnancy Proteins
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Survivin
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Placenta Growth Factor