Cdc42-mediated inhibition of GSK-3β improves angio-architecture and lumen formation during VEGF-driven pathological angiogenesis

Vascular endothelial growth factor-A (VEGF) typically induces abnormal angiogenesis in the adult, thereby aggravating disease pathology and limiting utility of VEGF for therapeutic angiogenesis. To identify strategies for rectifying defects in pathological VEGF neovessels, we investigated consequenc...

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Veröffentlicht in:	Microvascular research 2011-01, Vol.81 (1), p.34-43
Hauptverfasser:	Hoang, Mien V., Nagy, Janice A., Senger, Donald R.
Format:	Artikel
Sprache:	eng
Schlagworte:	Actin Cytoskeleton - metabolism Animals Blood Vessels - drug effects Blood Vessels - pathology Capillary morphogenesis Cdc42 cdc42 GTP-Binding Protein - genetics cdc42 GTP-Binding Protein - metabolism Cells, Cultured Cytoskeleton Endothelial cells Endothelial Cells - cytology Endothelial Cells - metabolism Female Glycogen Synthase Kinase 3 - antagonists & inhibitors Glycogen Synthase Kinase 3 - metabolism Glycogen Synthase Kinase 3 beta Glycogen synthase kinase-3β (GSK-3β) Humans Lumens Male Melanoma - blood supply Melanoma - metabolism Melanoma - pathology Mice Mice, Nude Microtubules - metabolism Neovascularization, Pathologic - metabolism Neovascularization, Pathologic - pathology Neovascularization, Physiologic - drug effects Neovascularization, Physiologic - physiology Pathological angiogenesis Phosphorylation - physiology Protein Kinase Inhibitors - pharmacology Thiadiazoles - administration & dosage Thiadiazoles - pharmacology Transduction, Genetic Transfection Vascular endothelial growth factor (VEGF) Vascular Endothelial Growth Factor A - genetics Vascular Endothelial Growth Factor A - metabolism
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