Gestational Diabetes Reduces Adenosine Transport in Human Placental Microvascular Endothelium, an Effect Reversed by Insulin

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dc.contributor.authorSalomon, Carlos
dc.contributor.authorWestermeier, Francisco
dc.contributor.authorPuebla, Carlos
dc.contributor.authorArroyo, Pablo
dc.contributor.authorGuzman Gutierrez, Enrique
dc.contributor.authorPardo, Fabian
dc.contributor.authorLeiva, Andrea
dc.contributor.authorCasanello, Paola
dc.contributor.authorSobrevia, Luis
dc.date.accessioned2024-01-10T13:13:21Z
dc.date.available2024-01-10T13:13:21Z
dc.date.issued2012
dc.description.abstractGestational diabetes mellitus (GDM) courses with increased fetal plasma adenosine concentration and reduced adenosine transport in placental macrovascular endothelium. Since insulin modulates human equilibrative nucleoside transporters (hENTs) expression/activity, we hypothesize that GDM will alter hENT2-mediated transport in human placental microvascular endothelium (hPMEC), and that insulin will restore GDM to a normal phenotype involving insulin receptors A (IR-A) and B (IR-B). GDM effect on hENTs expression and transport activity, and IR-A/IR-B expression and associated cell signalling cascades (p42/44 mitogen-activated protein kinases (p42/44(mapk)) and Akt) role in hPMEC primary cultures was assayed. GDM associates with elevated umbilical whole and vein, but not arteries blood adenosine, and reduced hENTs adenosine transport and expression. IR-A/IR-B mRNA expression and p42/44(mapk)/Akt ratios ('metabolic phenotype') were lower in GDM. Insulin reversed GDM-reduced hENT2 expression/activity, IR-A/IR-B mRNA expression and p42/44(mapk)/Akt ratios to normal pregnancies ('mitogenic phenotype'). It is suggested that insulin effects required IR-A and IR-B expression leading to differential modulation of signalling pathways restoring GDM-metabolic to a normal-mitogenic like phenotype. Insulin could be acting as protecting factor for placental microvascular endothelial dysfunction in GDM.
dc.description.funderFondo Nacional de Desarrollo Cientifico y Tecnologico
dc.description.funderComision Nacional de Investigacion en Ciencia y Tecnologia (CONICYT)
dc.description.funderPontificia Universidad Catolica de Chile (PUC), Chile
dc.description.funderCONICYT-PhD (Chile) fellowships
dc.description.funderPUC-PhD fellowship
dc.format.extent14 páginas
dc.fuente.origenWOS
dc.identifier.doi10.1371/journal.pone.0040578
dc.identifier.issn1932-6203
dc.identifier.pubmedidMEDLINE:22808198
dc.identifier.urihttps://doi.org/10.1371/journal.pone.0040578
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/78295
dc.identifier.wosidWOS:000306366400038
dc.information.autorucMedicina;Arroyo P;S/I;121667
dc.information.autorucMedicina;Casanello P;S/I;146772
dc.information.autorucCiencias Biológicas;Guzman E;S/I;197588
dc.information.autorucMedicina;Leiva A;S/I;3362
dc.information.autorucMedicina;Pardo F;S/I;1004392
dc.information.autorucCiencias Biológicas;Puebla C;S/I;124965
dc.information.autorucMedicina;Salomon C;S/I;189546
dc.information.autorucMedicina;Sobrevia L;S/I;1002656
dc.information.autorucCiencias Biológicas;Westermeier F;S/I;181374
dc.issue.numero7
dc.language.isoen
dc.nota.accesoSin adjunto
dc.publisherPUBLIC LIBRARY SCIENCE
dc.revistaPLOS ONE
dc.rightsregistro bibliográfico
dc.subjectRECEPTOR ISOFORMS
dc.subjectGLUCOSE
dc.subjectRESISTANCE
dc.subjectMELLITUS
dc.subjectDYSFUNCTION
dc.subjectEXPRESSION
dc.subjectPROTEIN-1
dc.subjectCELLS
dc.subject.ods03 Good Health and Well-being
dc.subject.ods05 Gender Equality
dc.subject.odspa03 Salud y bienestar
dc.subject.odspa05 Igualdad de género
dc.titleGestational Diabetes Reduces Adenosine Transport in Human Placental Microvascular Endothelium, an Effect Reversed by Insulin
dc.typeartículo
dc.volumen7
sipa.codpersvinculados121667
sipa.codpersvinculados146772
sipa.codpersvinculados197588
sipa.codpersvinculados3362
sipa.codpersvinculados1004392
sipa.codpersvinculados124965
sipa.codpersvinculados189546
sipa.codpersvinculados1002656
sipa.codpersvinculados181374
sipa.indexWOS
sipa.indexScopus
sipa.trazabilidadCarga SIPA;09-01-2024
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