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dc.contributor.authorOller, Jorge 
dc.contributor.authorAlfranca, Arantzazu 
dc.contributor.authorMendez-Barbero, Nerea 
dc.contributor.authorArmesilla, Angel Luis
dc.contributor.authorAlberca, Rut 
dc.contributor.authorEsteban, Vanesa 
dc.contributor.authorMartinez-Martinez, Sara 
dc.contributor.authorArroyo, Alicia G 
dc.contributor.authorMinami, Takashi
dc.contributor.authorCampanero, Miguel
dc.contributor.authorRedondo, Juan Miguel 
dc.date.accessioned2020-06-12T11:41:02Z
dc.date.available2020-06-12T11:41:02Z
dc.date.issued2014-04
dc.identifier.citation18th International Vascular Biology Meeting. 2014es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/10389
dc.description18th International Vascular Biology Meeting. Kyoto, 14-17 Apr. 2014es_ES
dc.description.abstractVascular remodeling consists of the structural alteration and arrangement of blood vessels. During this process cell migration, proliferation, cell death, and modifications in extracellular matrix (ECM) components are produced. It is present in major vascular diseases such as hypertension, aneurysm, vascular stenosis, and atherosclerosis. Vascular Endothelial Growth Factor (VEGF) and Angiotensin- II (Ang-II) major regulatory factors in vascular biology. VEGF induce endothelial cell migration and proliferation and contribute to pathophysiological angiogenesis. Ang-II is a potent vasoconstrictor agent, although it is also involved in inflammation, cell growth, vascular permeability and matrix deposition. In vivo, Ang-II administration induces aortic abdominal aneurysm (AAA) in ApoE KO mice, and increases restenosis and atherosclerosis. These processes are blocked by inhibition of the the calcium-calcineurin-NFAT signaling pathway. in response to increases in intracellular calcium, Calcineurin (CN) dephosphorylates NFAT transcription factors, thus, they become transcriptionally active. Some metalloproteinases are among VEGF/Ang-II-regulated genes, which participate in vascular remodeling, modifying ECM. Adamts-1 (A Disintegrin and Metalloproteinase with Thrombospondin motifs type I), mainly degrades proteoglycans. Mechanisms which regulate Adamts-1 gene expression during vascular remodeling have not been fully elucidated. Our findings indicate that VEGF and Ang-II increase Adamts-1 expression through differential signal transduction pathways, which specifically switch on the activity of NFAT or C/EBPβ transcription factors respectively, in both endothelial (EC) and smooth muscle cells (VSMCs).es_ES
dc.language.isoenges_ES
dc.relation.isversionofPreprintes_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.titleDifferential regulation of Adamts-1 gene expression by VEGF and Angiotensin-II in endothelial and vascular smooth muscle cellses_ES
dc.typePósteres_ES
dc.rights.licenseAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.description.peerreviewedNoes_ES
dc.repisalud.orgCNICCNIC::Grupos de investigación::Regulación Génica en Remodelado Vascular e Inflamaciónes_ES
dc.repisalud.institucionCNICes_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES


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Attribution-NonCommercial-NoDerivatives 4.0 Internacional
This item is licensed under a: Attribution-NonCommercial-NoDerivatives 4.0 Internacional