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dc.contributor.authorRobles-Vera, Iñaki
dc.contributor.authorToral Jiménez, Marta
dc.contributor.authorde la Visitación, Néstor
dc.contributor.authorAguilera Sánchez, Nazareth
dc.contributor.authorRedondo, Juan Miguel
dc.contributor.authorDuarte Pérez, Juan Manuel 
dc.date.accessioned2020-06-01T12:52:23Z
dc.date.available2020-06-01T12:52:23Z
dc.date.issued2020-04-16
dc.identifier.citationRobles-Vera I, Toral M, de la Visitación N, Aguilera-Sánchez N, Redondo JM and Duarte J (2020) Protective Effects of Short-Chain Fatty Acids on Endothelial Dysfunction Induced by Angiotensin II. Front. Physiol. 11:277. [doi: 10.3389/fphys.2020.00277]es_ES
dc.identifier.urihttp://hdl.handle.net/10481/62313
dc.descriptionThe Supplementary Material for this article can be found online at: https://www.frontiersin.org/articles/10.3389/fphys.2020.00277/full#supplementary-materiales_ES
dc.description.abstractShort-chain fatty acids (SCFAs) are among the main classes of bacterial metabolic products and are mainly synthesized in the colon through bacterial fermentation. Short-chain fatty acids, such as acetate, butyrate, and propionate, reduce endothelial activation induced by proinflammatory mediators, at least in part, by activation of G protein–coupled receptors (GPRs): GPR41 and GPR43. The objective of the study was to analyze the possible protective effects of SCFAs on endothelial dysfunction induced by angiotensin II (AngII). Rat aortic endothelial cells (RAECs) and rat aortas were incubated with AngII (1 μM) for 6 h in the presence or absence of SCFAs (5–10 mM). In RAECs, we found that AngII reduces the production of nitric oxide (NO) stimulated by calcium ionophore A23187; increases the production of reactive oxygen species (ROS), both from the nicotinamide adenine dinucleotide phosphate oxidase system and the mitochondria; diminishes vasodilator-stimulated phosphoprotein (VASP) phosphorylation at Ser239; reduces GPR41 and GPR43 mRNA level; and reduces the endothelium-dependent relaxant response to acetylcholine in aorta. Coincubation with butyrate and acetate, but not with propionate, increases both NO production and pSer239-VASP, reduces the concentration of intracellular ROS, and improves relaxation to acetylcholine. The beneficial effects of butyrate were inhibited by the GPR41 receptor antagonist, β-hydroxybutyrate, and by the GPR43 receptor antagonist, GLPG0794. Butyrate inhibited the down-regulation of GPR41 and GPR43 induced by AngII, being without effect acetate and propionate. Neither β-hydroxybutyrate nor GLPG0794 affects the protective effect of acetate in endothelial dysfunction. In conclusion, acetate and butyrate improve endothelial dysfunction induced by AngII by increasing the bioavailability of NO. The effect of butyrate seems to be related to GPR41/43 activation, whereas acetate effects were independent of GPR41/43.es_ES
dc.description.sponsorshipComision Interministerial de Ciencia y Tecnologia, Ministerio de Economia y competitividad SAF2017-8489-Res_ES
dc.description.sponsorshipJunta de Andalucia CTS164es_ES
dc.description.sponsorshipEuropean Union (EU)es_ES
dc.description.sponsorshipMinisterio de Economia y competitividad, Instituto de Salud Carlos III (CIBER-CV), Spaines_ES
dc.language.isoenges_ES
dc.publisherFrontiers Mediaes_ES
dc.rightsAtribución 3.0 España*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/*
dc.subjectEndothelial dysfunctiones_ES
dc.subjectShort chain fatty acidses_ES
dc.subjectNitric oxidees_ES
dc.subjectAngiotensin IIes_ES
dc.subjectOxidative stress es_ES
dc.titleProtective Effects of Short-Chain Fatty Acids on Endothelial Dysfunction Induced by Angiotensin IIes_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES
dc.identifier.doi10.3389/fphys.2020.00277


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Atribución 3.0 España
Except where otherwise noted, this item's license is described as Atribución 3.0 España