Your browser doesn't support javascript.
loading
Stimulation of receptor-mediated nitric oxide production by vanadate.
Hellermann, G R; Flam, B R; Eichler, D C; Solomonson, L P.
Afiliación
  • Hellermann GR; Department of Biochemistry and Molecular Biology, University of South Florida College of Medicine, Tampa, FL 33612-4799, USA. lsolomon@hsc.usf.edu
Arterioscler Thromb Vasc Biol ; 20(9): 2045-50, 2000 Sep.
Article en En | MEDLINE | ID: mdl-10978247
Nitric oxide (NO) production by endothelial cells in response to bradykinin (Bk) treatment was markedly and synergistically enhanced by cotreatment with sodium orthovanadate (vanadate), a phosphotyrosine phosphatase inhibitor. This enhancement was blocked by tyrosine kinase inhibitors. Calcium ionophore- (A23187) activated production of NO was also enhanced by cotreatment with vanadate. No significant changes were found in total endothelial NO synthase (eNOS) protein or in eNOS distribution between membrane (caveolae) and cytosolic fractions in response to the various treatments. Vanadate had no direct effect on eNOS activity, and lysates prepared from cells treated with vanadate showed little change in specific activity of eNOS. Western blots of immunoprecipitated eNOS showed the presence of a major tyrosine-phosphorylated protein band at a mass corresponding to approximately 125 kDa and 2 minor bands corresponding to approximately 105 and 75 kDa after treatment with vanadate/Bk. No tyrosine phosphorylation of eNOS after treatment with vanadate/Bk was observed. Geldanamycin, an inhibitor of heat shock protein 90, also inhibited the enhancement of NO production by vanadate/Bk or vanadate/A23187, and there was an increase in the amount of heat shock protein 90 that coimmunoprecipitated with eNOS after treatment with vanadate/Bk. These results show that there is a clear link between tyrosine phosphorylation and stimulation of eNO production, which does not appear to involve direct modification of eNOS, changes in eNOS levels, or compartmentation, but rather appears to be due to changes in proteins associating with eNOS, thereby enhancing the state of activation of eNOS.
Asunto(s)
Buscar en Google
Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Vanadatos / Proteínas Tirosina Fosfatasas / Péptidos y Proteínas de Señalización Intracelular / Inhibidores Enzimáticos / Óxido Nítrico Límite: Animals Idioma: En Revista: Arterioscler Thromb Vasc Biol Asunto de la revista: ANGIOLOGIA Año: 2000 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos
Buscar en Google
Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Vanadatos / Proteínas Tirosina Fosfatasas / Péptidos y Proteínas de Señalización Intracelular / Inhibidores Enzimáticos / Óxido Nítrico Límite: Animals Idioma: En Revista: Arterioscler Thromb Vasc Biol Asunto de la revista: ANGIOLOGIA Año: 2000 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos