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2003 | 50 | 1 |

Tytuł artykułu

Reciprocal regulation between nitric oxide and vascular endothelial growth factor in angiogenesis

Autorzy

Warianty tytułu

Języki publikacji

EN

Abstrakty

EN
Physiologically, angiogenesis is tightly regulated, or otherwise it leads to pathologi­cal processes, such as tumors, inflammatory diseases, gynecological diseases and dia­betic retinopathy. The vascular endothelial growth factor (VEGF) is a potent and criti­cal inducer of angiogenesis. The VEGF gene expression is regulated by a variety of stimuli. Hypoxia is one of the most potent inducers of the VEGF expression. The hypoxia inducible factor 1 (HIF-1) plays as a key transcription factor in hypo- xia-mediated VEGF gene upregulation. Nitric oxide (NO) as well as hypoxia is re­ported to upregulate the VEGF gene by enhancing HIF-1 activity. The Akt/protein kinase B (PKB) pathway may be involved in NO-mediated HIF-1 activation in limited cell lines. There are some reports of negative effects of NO on HIF-1 and VEGF activ­ity. These conflicting data of NO effects may be attributed mainly to the amount of re­leased NO. Indeed, NO can be a positive or negative modulator of the VEGF gene un­der the same conditions simply by changing its amounts. The VEGF-mediated angiogenesis requires NO production from activated endothelial NO synthase (eNOS). Activation of eNOS by VEGF involves several pathways including Akt/PKB, Ca2+ /calmodulin, and protein kinase C. The NO-mediated VEGF expression can be regulated by HIF-1 and heme oxygenase 1 (HO-1) activity, and the VEGF-mediated NO production by eNOS can be also modulated by HIF-1 and HO-1 activity, depending upon the amount of produced NO. These reciprocal relations between NO and VEGF may contribute to regulated angiogenesis in normal tissues.

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-

Rocznik

Tom

50

Numer

1

Opis fizyczny

p.49-59,fig.

Twórcy

autor
  • Center Research Institute East, Chiba, 277-8577, Japan
autor

Bibliografia

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