scholarly journals Thrombospondin‐1 modulates vascular endothelial growth factor activity at the receptor level

2009 ◽  
Vol 23 (10) ◽  
pp. 3368-3376 ◽  
Author(s):  
Xuefeng Zhang ◽  
Shideh Kazerounian ◽  
Mark Duquette ◽  
Carole Perruzzi ◽  
Janice A. Nagy ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Vascular Endothelial ◽  
Factor Activity ◽  
Receptor Level ◽  
Thrombospondin 1 ◽  
Endothelial Growth Factor

scholarly journals Multiple mechanisms for exogenous heparin modulation of vascular endothelial growth factor activity

2010 ◽  
Vol 111 (2) ◽  
pp. 461-468 ◽  
Author(s):  
Errol Wijelath ◽  
Mayumi Namekata ◽  
Jacqueline Murray ◽  
Mai Furuyashiki ◽  
Siyuan Zhang ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Vascular Endothelial ◽  
Factor Activity ◽  
Endothelial Growth Factor

scholarly journals Thrombospondin-1 Is Downregulated by Anoxia and Suppresses Tumorigenicity of Human Glioblastoma Cells

2000 ◽  
Vol 191 (10) ◽  
pp. 1789-1798 ◽  
Author(s):  
Mirna Tenan ◽  
Giulia Fulci ◽  
Michele Albertoni ◽  
Annie-Claire Diserens ◽  
Marie-France Hamou ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Blood Vessels ◽  
Vascular Endothelial ◽  
Glioblastoma Cell ◽  
Glioblastoma Cells ◽  
Thrombospondin 1 ◽  
Natural Inhibitor ◽  
Endothelial Growth Factor

Angiogenesis, the sprouting of new capillaries from preexisting blood vessels, results from a disruption of the balance between stimulatory and inhibitory factors. Here, we show that anoxia reduces expression of thrombospondin-1 (TSP-1), a natural inhibitor of angiogenesis, in glioblastoma cells. This suggests that reduced oxygen tension can promote angiogenesis not only by stimulating the production of inducers, such as vascular endothelial growth factor, but also by reducing the production of inhibitors. This downregulation may significantly contribute to glioblastoma development, since we show that an increase in TSP-1 expression is sufficient to strongly suppress glioblastoma cell tumorigenicity in vivo.

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