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Endoglin regulates cyclooxygenase-2 expression and activity

Authordc.contributor.authorJerkic, Mirjana 
Authordc.contributor.authorRivas Elena, Juan V. es_CL
Authordc.contributor.authorSantibáñez, Juan Francisco es_CL
Authordc.contributor.authorPrieto, Marta es_CL
Authordc.contributor.authorRodríguez Barbero, Alicia es_CL
Authordc.contributor.authorPérez Barriocanal, Fernando es_CL
Authordc.contributor.authorPericacho, Miguel es_CL
Authordc.contributor.authorArévalo, Miguel es_CL
Authordc.contributor.authorVary, Calvin P.H. es_CL
Authordc.contributor.authorLetarte, Michelle es_CL
Authordc.contributor.authorBernabeu, Carmelo es_CL
Authordc.contributor.authorLópez Novoa, José M. es_CL
Admission datedc.date.accessioned2009-04-13T17:34:14Z
Available datedc.date.available2009-04-13T17:34:14Z
Publication datedc.date.issued2006-08-04
Cita de ítemdc.identifier.citationCIRCULATION RESEARCH Volume: 99 Issue: 3 Pages: 248-256 Published: AUG 4 2006en
Identifierdc.identifier.issn0009-7330
Identifierdc.identifier.urihttp://repositorio.uchile.cl/handle/2250/123863
Abstractdc.description.abstractThe endoglin heterozygous (Eng(+/-)) mouse, which serves as a model of hereditary hemorrhagic telangiectasia (HHT), was shown to express reduced levels of endothelial NO synthase (eNOS) with impaired activity. Because of intricate changes in vasomotor function in the Eng(+/-) mice and the potential interactions between the NO- and prostaglandin-producing pathways, we assessed the expression and function of cyclooxygenase (COX) isoforms. A specific upregulation of COX-2 in the vascular endothelium and increased urinary excretion of prostaglandin E-2 were observed in the Eng(+/-) mice. Specific COX-2 inhibition with parecoxib transiently increased arterial pressure in Eng(+/-) but not in Eng(+/+) mice. Transfection of endoglin in L6E9 myoblasts, shown previously to stimulate eNOS expression, led to downregulation of COX-2 with no change in COX-1. In addition, COX-2 promoter activity and protein levels were inversely correlated with endoglin levels, in doxycyclin-inducible endothelial cells. Chronic NO synthesis inhibition with N-omega-nitro-L-arginine methyl ester induced a marked increase in COX-2 only in the normal Eng(+/+) mice. N-omega-nitro-L-arginine methyl ester also increased COX-2 expression and promoter activity in doxycyclin-inducible endoglin expressing endothelial cells, but not in control cells. The level of COX-2 expression following transforming growth factor-beta 1 treatment was less in endoglin than in mock transfected L6E9 myoblasts and was higher in human endothelial cells silenced for endoglin expression. Our results indicate that endoglin is involved in the regulation of COX-2 activity. Furthermore, reduced endoglin levels and associated impaired NO production may be responsible, at least in part, for augmented COX-2 expression and activity in the Eng(+/-) mice.en
Lenguagedc.language.isoenen
Publisherdc.publisherLIPPINCOTT WILLIAMS & WILKINSen
Keywordsdc.subjectGROWTH-FACTOR-BETAen
Títulodc.titleEndoglin regulates cyclooxygenase-2 expression and activityen
Document typedc.typeArtículo de revistaen


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