A Role for Insulin on L-Arginine Transport in Fetal Endothelial Dysfunction in Hyperglycaemia

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dc.contributor.authorSobrevia, Luis
dc.contributor.authorGonzalez, Marcelo
dc.date.accessioned2024-01-10T12:37:39Z
dc.date.available2024-01-10T12:37:39Z
dc.date.issued2009
dc.description.abstractEndothelial cells are key in the regulation of vascular tone through the release of vasoactive molecules, including nitric oxide (NO). NO is a gas synthesized from the cationic amino acid L-arginine via the endothelial NO synthase (eNOS). The semi-essential amino acid L-arginine is a taken up by endothelial cells via systems y(+) and y(+)L in primary cultures of human umbilical vein endothelial cells (HUVEC). System y(+) is a family of membrane transporters including at least five transport systems for cationic amino acids (CAT) of which HUVEC express human CAT-1 (hCAT-1) and hCAT-2B. Exposure of HUVEC to high extracellular concentrations of D-glucose increases L-arginine transport, hCAT-1 mRNA expression and eNOS activity. These phenomena are also related with increased production of reactive oxygen species (ROS), thus supporting the possibility that changes in L-arginine/NO signalling pathway result from elevated ROS. It has been shown that insulin blocks D-glucose-increased L-arginine transport and cGMP accumulation in HUVEC, whereas in this cell type insulin also modulates high D-glucose effects by activating the transcriptional factors Sp1 and NF kappa B. These transcription factors have response elements in SLC7A1 (for hCAT-1) gene promoter region, thus representing 2 possible targets for regulation of the expression of this transporter by D-glucose and/or insulin in this cell type. Recent evidences suggest that insulin blocks the stimulatory effect of D- glucose on L-arginine transport by reducing the transcriptional activity of SLC7A1 via Sp1-, NF kappa B- and ROS-dependent mechanisms. Thus, a role for these transcription factors in response to insulin is proposed in fetal endothelial cells exposed to hyperglycaemia.
dc.description.funderFondo Nacional de Desarrollo Cientifico y Tecnologico (FONDECYT)
dc.description.funderComision Nacional de Ciencia y Tecnolog a (CONICYT)
dc.fechaingreso.objetodigital2024-05-17
dc.format.extent8 páginas
dc.fuente.origenWOS
dc.identifier.doi10.2174/157016109789043919
dc.identifier.eissn1875-6212
dc.identifier.issn1570-1611
dc.identifier.pubmedidMEDLINE:19485892
dc.identifier.urihttps://doi.org/10.2174/157016109789043919
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/76895
dc.identifier.wosidWOS:000269248200006
dc.information.autorucMedicina;Sobrevia L;S/I;1002656
dc.issue.numero4
dc.language.isoen
dc.nota.accesocontenido parcial
dc.pagina.final474
dc.pagina.inicio467
dc.publisherBENTHAM SCIENCE PUBL LTD
dc.revistaCURRENT VASCULAR PHARMACOLOGY
dc.rightsacceso restringido
dc.subjectGlucose
dc.subjecthyperglycaemia
dc.subjectdiabetes
dc.subjectL-arginine
dc.subjecttransport
dc.subjecthuman
dc.subjectendothelium
dc.subjectNF-KAPPA-B
dc.subjectDNA-BINDING EFFICIENCY
dc.subjectNITRIC-OXIDE SYNTHESIS
dc.subjectHIGH GLUCOSE
dc.subjectAMINO-ACID
dc.subjectTRANSCRIPTIONAL REGULATION
dc.subjectADENOSINE TRANSPORT
dc.subjectFIBRONECTIN SYNTHESIS
dc.subjectDEPENDENT RELAXATION
dc.subjectOXIDATIVE STRESS
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleA Role for Insulin on L-Arginine Transport in Fetal Endothelial Dysfunction in Hyperglycaemia
dc.typeartículo
dc.volumen7
sipa.codpersvinculados1002656
sipa.indexWOS
sipa.indexScopus
sipa.trazabilidadCarga SIPA;09-01-2024
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