Placental growth factor induces FosB and c‐Fos gene expression via Flt‐1 receptors

@article{Holmes2004PlacentalGF,
  title={Placental growth factor induces FosB and c‐Fos gene expression via Flt‐1 receptors},
  author={David Ian Roderick Holmes and Ian C. Zachary},
  journal={FEBS Letters},
  year={2004},
  volume={557}
}
Placenta Growth Factor is a Survival Factor for Human Malignant Mesothelioma Cells
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Dihydroartemisinin downregulates vascular endothelial growth factor expression and induces apoptosis in chronic myeloid leukemia K562 cells
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PIGF Knockout Delays Brain Vessel Growth and Maturation upon Systemic Hypoxic Challenge
TLDR
Vascular endothelial growth factor expression levels were found to be significantly lower in the frontal cortex of Pl GF−/− compared with those in PlGF+/+ animals during the first 5 days of hypoxia, which in combination with the lack of PlGF may have contributed to the delayed angiogenic response and the prothrombotic phenotype observed in the PlGF −/−animals.
VEGF/VEGFR2 Signaling Regulates Germ Cell Proliferation in vitro and Promotes Mouse Testicular Regeneration in vivo
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Data suggest that VEGF/VEGFR2 signaling regulates germ cell proliferation and promotes testicular regeneration via direct action on germ cells and the enhancement of vascularization.
RGS13 acts as a nuclear repressor of CREB.
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Placenta growth factor stimulates MAP kinase and mitogenicity but not phospholipase C-γ and migration of endothelial cells expressing Flt 1
TLDR
Flt 1 is able to mediate an array of biological signals when appropriately stimulated and that the pattern of responses of PlGF-stimulation of Flt 1 is distinct from thepattern of responses to VEGF- Stimulation of KDR.
The Vascular Endothelial Growth Factor Receptor Flt-1 Mediates Biological Activities
TLDR
Findings strongly suggest Flt-1 as a functional receptor for VEGF and PlGF in monocytes and endothelial cells and identify this receptor as a mediator of monocyte recruitment and procoagulant activity.
Role of VEGF receptor-1 (Flt-1) in mediating calcium-dependent nitric oxide release and limiting DNA synthesis in human trophoblast cells.
TLDR
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.
Synergism between vascular endothelial growth factor and placental growth factor contributes to angiogenesis and plasma extravasation in pathological conditions
TLDR
It is reported that embryonic angiogenesis in mice was not affected by deficiency of PlGF, andTransplantation of wild-type bone marrow rescued the impairedAngiogenesis and collateral growth in Pgf−/− mice, indicating that PlGF might have contributed to vessel growth in the adult by mobilizing bone-marrow–derived cells.
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Analysis of Biological Effects and Signaling Properties of Flt-1 (VEGFR-1) and KDR (VEGFR-2)
TLDR
KDR-selective V EGF was also able to induce angiogenesis in the rat cornea to an extent indistinguishable from wild type VEGF, and it is demonstrated that KDR, but not Flt-1, stimulation is responsible for the induction of vascular permeability by VEGf.
Vascular Endothelial Growth Factor–Regulated Gene Expression in Endothelial Cells: KDR-Mediated Induction of Egr3 and the Related Nuclear Receptors Nur77, Nurr1, and Nor1
TLDR
The genes identified here are novel candidates as key early mediators of VEGF-induced endothelial functions.
Role of the Flt-1 receptor tyrosine kinase in regulating the assembly of vascular endothelium
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It is reported that Flt-1 is essential for the organization of embryonic vasculature, but is not essential for endothelial cell differentiation, and it is suggested that the FlT-1 signalling pathway may regulate normal endothelium cell-cell or cell-matrix interactions during vascular development.
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