Placenta

dc.creatorSalsoso-Rodríguez, María Rocío
dc.creatorGuzmán-Gutiérrez, E
dc.creatorSáez-Gutiérrez, Tamara Andrea
dc.creatorBugueño, K
dc.creatorRamirez, M A
dc.creatorPardo, Fabián
dc.creatorLeiva, Andrea
dc.creatorSanhueza, C
dc.creatorMate, A
dc.creatorVázquez, C
dc.creatorSobrevia-Luarte, Luis Alberto
dc.date2019-06-25T21:50:12Z
dc.date2022-07-07T21:48:16Z
dc.date2019-06-25T21:50:12Z
dc.date2022-07-07T21:48:16Z
dc.date2015
dc.date.accessioned2023-08-21T21:48:24Z
dc.date.available2023-08-21T21:48:24Z
dc.identifier1150377
dc.identifier1150377
dc.identifierhttps://hdl.handle.net/10533/236143
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8286562
dc.descriptionIntroduction: Preeclampsia is associated with impaired placental vasodilation and reduced endothelial nitric oxide synthase (eNOS) activity in the foetoplacental circulation. Adenosine and insulin stimulate vasodilation in endothelial cells, and this activity is mediated by adenosine receptor activation in uncomplicated pregnancies; however, this activity has yet to be examined in preeclampsia. Early onset preeclampsia is associated with severe placental vasculature alterations that lead to altered foetus growth and development, but whether late-onset preeclampsia (LOPE) alters foetoplacental vascular function is unknown. Methods: Vascular reactivity to insulin (0.1-1000 nmol/L, 5 min) and adenosine (1 mmol/L, 5 min) was measured in KCI-preconstricted human umbilical vein rings from normal and LOPE pregnancies using a wire myograph. The protein levels of human cationic amino acid transporter 1 (hCAT-1), adenosine receptor subtypes, total and Ser(1177)-or Thr(495)-phosphorylated eNOS were detected via Western blot, and L-arginine transport (0-1000 mu mol/L L-arginine, 3 mu Ci/mL L-[H-3]arginine, 20 s, 37 degrees C) was measured in the presence or absence of insulin and adenosine receptor agonists or antagonists in human umbilical vein endothelial cells (HUVECs) from normal and LOPE pregnancies. Results: LOPE increased the maximal L-arginine transport capacity and hCAT-1 and eNOS expression and activity compared with normal conditions. The A(2A) adenosine receptor (A(2A)AR) antagonist ZM-241385 blocked these effects of LOPE. Insulin-mediated umbilical vein ring relaxation was lower in LOPE pregnancies than in normal pregnancies and was restored using the A(2A)AR antagonist. Discussion and conclusions: The reduced foetoplacental vascular response to insulin may result from A(2A)AR activation in LOPE pregnancies. (C) 2014 Elsevier Ltd. All rights reserved. Keywords. Author Keywords:Preeclampsia; Foetal endothelium; Arginine; Insulin; Adenosine receptor
dc.relationinstname: Conicyt
dc.relationreponame: Repositorio Digital RI2.0
dc.relationinfo:eu-repo/grantAgreement//1150377
dc.relationinfo:eu-repo/semantics/dataset/hdl.handle.net/10533/93477
dc.relationhttps://www.sciencedirect.com/science/article/pii/S0143400414009072
dc.rightsinfo:eu-repo/semantics/openAccess
dc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile
dc.rightsinfo:eu-repo/semantics/openAccess
dc.rightshttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/
dc.titleInsulin restores L-arginine transport requiring adenosine receptors activation in umbilical vein endothelium from late-onset preeclampsia
dc.titlePlacenta
dc.typeArticulo
dc.typeinfo:eu-repo/semantics/article
dc.typeinfo:eu-repo/semantics/publishedVersion


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