Endostatin induces acute endothelial nitric oxide and prostacyclin release

Chunying Li, M. Brennan Harris, Virginia J. Venema, Richard C Venema

Research output: Contribution to journalArticle

19 Scopus citations

Abstract

Chronic exposure to endostatin (ES) blocks endothelial cell (EC) proliferation, and migration and induces EC apoptosis thereby inhibiting angiogenesis. Nitric oxide (NO) and prostacyclin (PGI2), in contrast, play important roles in promoting angiogenesis. In this study, we examined the acute effects of ES on endothelial NO and PGI2 production. Unexpectedly, a cGMP reporter cell assay showed that ES-induced acute endothelial NO release in cultured bovine aortic endothelial cells (BAECs). Enzyme immunoassay showed that ES also induced an acute increase in PGI 2 production in BAECs. These results were confirmed by ex vivo vascular ring studies that showed vascular relaxation in response to ES. Immunoblot analysis showed that ES stimulated acute phosphorylation of endothelial nitric oxide synthase (eNOS) at Ser116, Ser617, Ser635, and Ser1179, and dephosphorylation at Thr497 in BAECs, events associated with eNOS activation. Short-term exposure of EC to ES, therefore, unlike long-term exposure which is anti-angiogenic, may be pro-angiogenic.

Original languageEnglish (US)
Pages (from-to)873-878
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume329
Issue number3
DOIs
StatePublished - Apr 15 2005

Keywords

  • Endostatin
  • Nitric oxide release
  • Phosphorylation
  • eNOS

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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