Effect of Placenta Growth Factor-1 on Proliferation and Release of Nitric Oxide, Cyclic AMP and Cyclic GMP in Human Epithelial Cells Expressing the FLT-1 Receptor

  title={Effect of Placenta Growth Factor-1 on Proliferation and Release of Nitric Oxide, Cyclic AMP and Cyclic GMP in Human Epithelial Cells Expressing the FLT-1 Receptor},
  author={Cristiana Angelucci and Gina Lama and Fortunata Iacopino and Domenico Maglione and Gigliola Sica},
  journal={Growth Factors},
  pages={193 - 206}
We investigated the effect of placenta growth factor-1 (PlGF-1) on cell growth and on the release of nitric oxide (NO), cyclic AMP (cAMP) and cyclic GMP (cGMP) in human malignant epithelial cells. A noteworthy increase in proliferation was induced in choriocarcinoma cells (BeWo) by PlGF-1 treatment, while breast cancer cells (CG-5) were minimally affected. Western blotting and immunocytochemistry demonstrated the expression of the PlGF-1 receptor fms-like tyrosine kinase-1 (Flt-1) in these… 
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Role of VEGF receptor-1 (Flt-1) in mediating calcium-dependent nitric oxide release and limiting DNA synthesis in human trophoblast cells.
It is reported that human trophoblast and endothelial cells contain functional Flt-1 receptors for VEGF that trigger the synthesis and release of nitric oxide (NO) by the activation of constitutive NO synthase (cNOS) and the contingency of this process on tyrosine phosphorylation and extracellular calcium is suggested.
Differential regulation of vascular endothelial growth factor and its receptor fms-like-tyrosine kinase is mediated by nitric oxide in rat renal mesangial cells.
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Protein Kinase G Mediates Vascular Endothelial Growth Factor-induced Raf-1 Activation and Proliferation in Human Endothelial Cells*
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Flt-1 but not KDR/Flk-1 tyrosine kinase is a receptor for placenta growth factor, which is related to vascular endothelial growth factor.
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Co-expression of vascular endothelial growth factor (VEGF) and its receptors (flk-1 and flt-1) in hormone-induced mammary cancer in the Noble rat
The present study is the first report showing that VEGF may act as a growth stimulator for mammary cancer cells in vivo and this autocrine regulatory role may be mediated through flk-1.
Nitric oxide mediates mitogenic effect of VEGF on coronary venular endothelium.
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Nitric Oxide Is an Upstream Signal of Vascular Endothelial Growth Factor-induced Extracellular Signal-regulated Kinase½ Activation in Postcapillary Endothelium*
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Nitric oxide causes apoptosis in pulmonary vascular smooth muscle cells.
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