Insulin restores glucose inhibition of adenosine transport by increasing the expression and activity of the equilibrative nucleoside transporter 2 in human umbilical vein endothelium

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dc.contributor.authorMunoz, Gonzalo
dc.contributor.authorSan Martin, Rody
dc.contributor.authorFarias, Marcelo
dc.contributor.authorCea, Luis
dc.contributor.authorVecchiola, Andrea
dc.contributor.authorCasanello, Paola
dc.contributor.authorSobrevia, Luis
dc.date.accessioned2024-01-10T13:13:56Z
dc.date.available2024-01-10T13:13:56Z
dc.date.issued2006
dc.description.abstractL-Arginine transport and nitric oxide (NO) synthesis (L-arginine/NO pathway) are stimulated by insulin, adenosine or elevated extracellular D-glucose in human umbilical vein endothelial cells (HUVEC). Adenosine uptake via the human equilibrative nucleoside transporters 1 (hENT1) and 2 (hENT2) has been proposed as a mechanism regulating adenosine plasma concentration, and therefore its vascular effects in human umbilical veins. Thus, altered expression and/or activity of hENT1 or hENT2 could lead to abnormal physiological plasma adenosine level. We have characterized insulin effect on adenosine transport in HUVEC cultured in normal (5 mM) or high (25, mM) D-glucose. Insulin (1 nM) increased overall adenosine transport associated with higher hENT2-, but lower hENT1-mediated transport in normal D-glucose. insulin increased hENT2 protein abundance in normal or high D-glucose, but reduced hENT1 protein abundance in normal D-glucose. Insulin did not alter the reduced hENT1 protein abundance, but blocked the reduced hENT1 and hENT2 mRNA expression induced by high D-glucose. Insulin effect on hENT1 mRNA expression in normal D-glucose was blocked by N-G-nitro-L-arginine methyl ester (L-NAME, NO synthase inhibitor) and mimicked by S-nitroso-N-acetyl-L,D-penicillamine (SNAP, NO donor). L-NAME did not block insulin effect on hENT2 expression. In conclusion, insulin stimulation of overall adenosine transport results from increased hENT2 expression and activity via a NO-independent mechanism. These findings could be important in hyperglycemia-associated pathological pregnancies, such as gestational diabetes, where plasma adenosine removal by the endothelium is reduced, a condition that could alter the blood flow from the placenta to the fetus affecting fetus growth and development. J. Cell. Physiol. 209: 826-835, 2006. (c) 2006 Wiley-Liss, Inc.
dc.fechaingreso.objetodigital2024-04-27
dc.format.extent10 páginas
dc.fuente.origenWOS
dc.identifier.doi10.1002/jcp.20769
dc.identifier.eissn1097-4652
dc.identifier.issn0021-9541
dc.identifier.pubmedidMEDLINE:16924660
dc.identifier.urihttps://doi.org/10.1002/jcp.20769
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/78355
dc.identifier.wosidWOS:000241754600033
dc.information.autorucMedicina;Casanello P;S/I;146772
dc.information.autorucFacultad de Medicina; Farias Jofre, Marcelo Enrique; S/I; 12286
dc.issue.numero3
dc.language.isoen
dc.nota.accesoContenido parcial
dc.pagina.final835
dc.pagina.inicio826
dc.publisherWILEY
dc.revistaJOURNAL OF CELLULAR PHYSIOLOGY
dc.rightsacceso restringido
dc.subjectNITRIC-OXIDE SYNTHESIS
dc.subjectL-ARGININE TRANSPORT
dc.subjectMESSENGER-RNA EXPRESSION
dc.subjectRAT T-LYMPHOCYTES
dc.subjectB-LYMPHOCYTES
dc.subjectUP-REGULATION
dc.subjectCELLS
dc.subjectLEVEL
dc.subjectRECEPTORS
dc.subjectPATHWAY
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleInsulin restores glucose inhibition of adenosine transport by increasing the expression and activity of the equilibrative nucleoside transporter 2 in human umbilical vein endothelium
dc.typeartículo
dc.volumen209
sipa.codpersvinculados146772
sipa.codpersvinculados12286
sipa.indexWOS
sipa.indexScopus
sipa.trazabilidadCarga SIPA;09-01-2024
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