Hypoxia increases equilibrative nucleoside transporter 2 activity by a transcriptional independent mechanism in human umbilical vein endothelium

dc.contributor.authorTorres, A
dc.contributor.authorSan Martin, R
dc.contributor.authorFarías Jofré, Marcelo Enrique
dc.contributor.authorSobrevía Luarte, Luis Alberto
dc.contributor.authorCasanello Toledo, Paola Cecilia
dc.date.accessioned2023-06-30T20:35:12Z
dc.date.available2023-06-30T20:35:12Z
dc.date.issued2006
dc.description.abstractLow oxygen tension (hypoxia) reduces adenosine transport in several types of mammalian cells. Adenosine transport is mediated by human equilibrative nucleoside transporter 1 (hENT1) and hENT2 in human umbilical vein endothelium (HUVEC), a fetal cell type that grows under 5% O2 (ie. normoxia for this cell type). We studied whether hypoxia alters hENT2 expression and activity in HUVEC. Methods: Cells were cultured (0-24 h) in 5% or 2% O2 (hypoxia), and [3H]adenosine uptake (125 and 500 μM, 4 μCi/ml, 20 s, 37°C) was measured in absence or presence of 100 nM nitrobenzylthioinosine (NBMPR, hENT1 inhibitor). hENT2 mRNA was quantified by real time RT-PCR, and protein abundance was determined by Western blot. SLC29A2 (for hENT2) promoter activity was measured following transfection (electroporation, 320 V, 30 ms) with pGL3 basic plasmid (firefly/renilla luciferase reporter gene) carrying -1477 bp and -587 bp of the promoter sequence. Results: Hypoxia reduced hENT2 mRNA expression (~55%), and promoter activity (~50%), but did not alter hENT2 protein abundance. Adenosine uptake via hENT2 was increased (2-fold) in hypoxia. Conclusions: Adenosine uptake via hENT2 may be modulated by post-translational mechanisms in hypoxia in HUVEC. Supported by FONDECYT 1030781/1030607/7050030. A Torres holds a School of Medicine research fellowship, and M Farías holds a CONICYT-PhD fellowship.
dc.fechaingreso.objetodigital2023-06-13
dc.format.extent1 página
dc.fuente.origenORCID
dc.identifier.doi10.1016/j.placenta.2005.10.001
dc.identifier.issn0143-4004
dc.identifier.urihttps://doi.org/10.1016/j.placenta.2005.10.001
dc.identifier.urihttps://publons.com/wos-op/publon/18766770/
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/74017
dc.information.autorucEscuela de Medicina ; Farías Jofré, Marcelo Enrique ; 0000-0003-0473-2295 ; 12286
dc.information.autorucEscuela de Medicina ; Sobrevía Luarte, Luis Alberto ; 0000-0001-5802-2243 ; 1002656
dc.information.autorucEscuela de Medicina ; Casanello Toledo, Paola Cecilia ; 0000-0002-2355-1476 ; 146772
dc.issue.numero1
dc.language.isoen
dc.nota.accesoContenido parcial
dc.pagina.finalA70
dc.pagina.inicioA70
dc.relation.ispartof2° Latinamerican Symposium on Fetal-Maternal Interaction and Placenta and XIX Annual Meeting of The Chilean Society of Physiological Sciences (2005 ; Santiago ; Chile)
dc.revistaPlacenta
dc.rightsacceso restringido
dc.titleHypoxia increases equilibrative nucleoside transporter 2 activity by a transcriptional independent mechanism in human umbilical vein endothelium
dc.typecomunicación de congreso
dc.volumen27
sipa.codpersvinculados12286
sipa.codpersvinculados1002656
sipa.codpersvinculados146772
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