scholarly journals Blockade of Vascular Endothelial Cell Growth Factor Receptor Signaling Is Sufficient to Completely Prevent Retinal Neovascularization

2000 ◽  
Vol 156 (2) ◽  
pp. 697-707 ◽  
Author(s):  
Hiroaki Ozaki ◽  
Man-Seong Seo ◽  
Keiko Ozaki ◽  
Haruhiko Yamada ◽  
Eri Yamada ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Growth Factor ◽  
Cell Growth ◽  
Vascular Endothelial Cell ◽  
Growth Factor Receptor ◽  
Vascular Endothelial ◽  
Endothelial Cell Growth Factor ◽  
Growth Factor Receptor Signaling ◽  
Endothelial Cell Growth ◽  
Cell Growth Factor Receptor

scholarly journals Cheiradone: a vascular endothelial cell growth factor receptor antagonist

2008 ◽  
Vol 9 (1) ◽  
pp. 7 ◽  
Author(s):  
Sajjad Hussain ◽  
Mark Slevin ◽  
Mohammad A Mesaik ◽  
Mohammad I Choudhary ◽  
Abdul H Elosta ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Growth Factor ◽  
Cell Growth ◽  
Receptor Antagonist ◽  
Vascular Endothelial Cell ◽  
Growth Factor Receptor ◽  
Vascular Endothelial ◽  
Endothelial Cell Growth Factor ◽  
Endothelial Cell Growth ◽  
Cell Growth Factor Receptor

scholarly journals Vascular Endothelial Cell Growth Factor A Acts via Platelet-Derived Growth Factor Receptor α To Promote Viability of Cells Enduring Hypoxia

2016 ◽  
Vol 36 (18) ◽  
pp. 2314-2327 ◽  
Author(s):  
Steven Pennock ◽  
Leo A. Kim ◽  
Andrius Kazlauskas
Keyword(s):  
Endothelial Cell ◽  
Growth Factor ◽  
Cell Growth ◽  
Vascular Endothelial Cell ◽  
Growth Factor Receptor ◽  
Platelet Derived Growth Factor ◽  
Vegf Receptor ◽  
Vascular Endothelial ◽  
Endothelial Cell Growth Factor ◽  
Endothelial Cell Growth

Vascular endothelial cell growth factor A (VEGF) is a biologically and therapeutically important growth factor because it promotes angiogenesis in response to hypoxia, which underlies a wide variety of both physiological and pathological settings. We report here that both VEGF receptor 2 (VEGFR2)-positive and -negative cells depended on VEGF to endure hypoxia. VEGF enhanced the viability of platelet-derived growth factor receptor α (PDGFRα)-positive and VEGFR2-negative cells by enabling indirect activation of PDGFRα, thereby reducing the level of p53. We conclude that the breadth of VEGF's influence extends beyond VEGFR-positive cells and propose a plausible mechanistic explanation of this phenomenon.

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