Nitric oxide reduces adenosine transporter ENT1 gene (SLC29A1) promoter activity in human fetal endotheliurn from gestational diabetes

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dc.contributor.authorFarias, Marcelo
dc.contributor.authorMartin, Rody San
dc.contributor.authorPuebla, Carlos
dc.contributor.authorPearson, Jeremy D.
dc.contributor.authorCasado, Javier F.
dc.contributor.authorPastor Anglada, Marcal
dc.contributor.authorCasanello, Paola
dc.contributor.authorSobrevia, Luis
dc.date.accessioned2024-01-10T13:51:10Z
dc.date.available2024-01-10T13:51:10Z
dc.date.issued2006
dc.description.abstractHuman umbilical vein endothelial cells (HUVEC) from gestational diabetes exhibit reduced adenosine uptake and increased nitric oxide (NO) synthesis. Adenosine transport via human equilibrative nucleoside transporters 1 (hENT1) is reduced by NO by unknown mechanisms in HUVEC. We examined whether gestational diabetes-reduced adenosine transport results from lower hENT1 gene (SLC29A1) expression. HUVEC from gestational diabetes exhibit reduced SLC29A1 promoter activity when transfected with pGL3-hENT1(-2154) compared with pGL3-hENT1(-1114) constructs, an effect blocked by N-G-nitro-L-arginine methyl ester (L-NAME, NOS inhibitor), but unaltered by S-nitroso-N-acetyl-L,D-penicillamine (SNAP, NO donor). In cells from gestational diabetes transfected with pGL3-hENT1(-2114), L-NAME increased, but SNAP did not alter promoter activity and hENT1 expression. However, in cells from normal pregnancies L-NAME increased, but SNAP reduced promoter activity and hENT1 expression. Adenovirus-silenced eNOS expression increased hENT1 expression and activity in cells from normal or gestational diabetic pregnancies. Thus, reduced adenosine transport may result from downregulation of SLC29A1 expression by NO in HUVEC from gestational diabetes. These findings explain the accumulation of extracellular adenosine detected in cultures of HUVEC from gestational diabetes. In addition, fetal endothelial dysfunction could be involved in the abnormal fetal development and growth seen in gestational diabetes.
dc.fechaingreso.objetodigital2024-04-27
dc.format.extent10 páginas
dc.fuente.origenWOS
dc.identifier.doi10.1002/jcp.20680
dc.identifier.eissn1097-4652
dc.identifier.issn0021-9541
dc.identifier.pubmedidMEDLINE:16688763
dc.identifier.urihttps://doi.org/10.1002/jcp.20680
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/79582
dc.identifier.wosidWOS:000238775100022
dc.information.autorucMedicina;Casanello P;S/I;146772
dc.information.autorucMedicina;Sobrevia L;S/I;1002656
dc.information.autorucFacultad de Medicina; Farias Jofre, Marcelo Enrique; S/I; 12286
dc.issue.numero2
dc.language.isoen
dc.nota.accesoContenido parcial
dc.pagina.final460
dc.pagina.inicio451
dc.publisherWILEY
dc.revistaJOURNAL OF CELLULAR PHYSIOLOGY
dc.rightsacceso restringido
dc.subjectUMBILICAL VEIN ENDOTHELIUM
dc.subjectCELLS
dc.subjectEXPRESSION
dc.subjectINHIBITION
dc.subjectHYPOXIA
dc.subjectSYNTHASE
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleNitric oxide reduces adenosine transporter ENT1 gene (SLC29A1) promoter activity in human fetal endotheliurn from gestational diabetes
dc.typeartículo
dc.volumen208
sipa.codpersvinculados146772
sipa.codpersvinculados1002656
sipa.codpersvinculados12286
sipa.indexWOS
sipa.indexScopus
sipa.trazabilidadCarga SIPA;09-01-2024
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