Gestational Diabetes and the Adenosine/L-Arginine/Nitric Oxide (ALANO) Pathway in Human Umbilical Vein Endothelium

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dc.catalogadorpau
dc.contributor.authorSan Martín, R.
dc.contributor.authorSobrevía Luarte, Luis Alberto
dc.date.accessioned2023-05-18T19:49:46Z
dc.date.available2023-05-18T19:49:46Z
dc.date.issued2006
dc.description.abstractAltered endothelial cell function is a key factor associated with vascular disorders and is critical in the fetal growth and development. Pregnancies affected by diseases such as gestational diabetes are associated with human umbilical vein endothelial dysfunction, a finding that has been associated with a high incidence of vascular complications during the adult life. Limited information is available addressing cellular mechanisms associated with altered human umbilical vein endothelial function in gestational diabetes. One of the key signalling pathways associated with altered vascular physiology is the synthesis of the vasodilator nitric oxide (NO) from the cationic amino acid L-arginine by the endothelium (i.e. the endothelial L-arginine/NO pathway). The activity of this signalling pathway is modulated by D-glucose, adenosine, insulin, and ATP, among other molecules, and is upregulated (transcriptional, post-transcriptional and post-translational levels) in gestational diabetes. This review focuses on the cellular and molecular mechanisms involved with elevated adenosine levels in fetal umbilical vein blood and the endothelial L-arginine/NO pathway activity in gestational diabetes. We suggest that a lower capacity of adenosine transport by the fetal endothelium in gestational diabetes leads to extracellular accumulation of this nucleoside and its higher bio-availability activates endothelial P1 type purinoceptors. A functional association between A2a purinoceptor subtype signalling and the activity of the L-arginine transport mediated by human cationic amino acid transporters and endothelial NO synthase activity (i.e. ‘ALANO pathway’) is proposed, revealing in part the mechanisms that account for human umbilical vein endothelial cell dysfunction programmed through the development of the fetus in gestational diabetes.
dc.format.extent10 páginas
dc.fuente.origenORCID
dc.identifier.doi10.1016/j.placenta.2005.01.011
dc.identifier.urihttps://doi.org/10.1016/j.placenta.2005.01.011
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/67117
dc.identifier.wosidWOS:000233996200001
dc.information.autorucEscuela de medicina; Sobrevía Luarte, Luis Alberto; 0000-0001-5802-2243; 1002656
dc.language.isoen
dc.nota.accesoContenido parcial
dc.pagina.final10
dc.pagina.inicio1
dc.revistaPlacenta
dc.rightsacceso restringido
dc.subject.ods03 Good health and well-being
dc.subject.odspa03 Salud y bienestar
dc.titleGestational Diabetes and the Adenosine/L-Arginine/Nitric Oxide (ALANO) Pathway in Human Umbilical Vein Endothelium
dc.typeartículo
dc.volumen27
sipa.codpersvinculados1002656
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