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http://hdl.handle.net/10261/117076
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Campo DC | Valor | Lengua/Idioma |
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dc.contributor.author | Roqué, Mercé | - |
dc.contributor.author | Novensà, Laura | - |
dc.contributor.author | Cidad, Pilar | - |
dc.contributor.author | Batle, Montserrat | - |
dc.contributor.author | Miguel-Velado, Eduardo | - |
dc.contributor.author | Alonso, Esperanza | - |
dc.contributor.author | Pérez-García, M. Teresa | - |
dc.contributor.author | López-López, José R. | - |
dc.contributor.author | Heras, Magda | - |
dc.date.accessioned | 2015-06-24T11:17:00Z | - |
dc.date.available | 2015-06-24T11:17:00Z | - |
dc.date.issued | 2012 | - |
dc.identifier.citation | ACC-12 | es_ES |
dc.identifier.uri | http://hdl.handle.net/10261/117076 | - |
dc.description | Resumen del póster presentado al American College of Cardiology - 61st Annual Scientific Seesion & Expo celebrado en Chicago (US) del 24 al 27 de marzo de 2012. | es_ES |
dc.description.abstract | [Background]: Vascular smooth muscle cells (VSMCs) are able to switch from a contractile to a proliferative phenotype, and this process is central to intimal hyperplasia formation. Phenotypic modulation requires a change in gene expression profile, including a switch in ion transport mechanisms. Potassium (K+) channels have been suggested to have a role in the processes of cell proliferation. Changes in K+ channels expression are associated with functional changes in the electrophysiological properties of VSMCs, which are linked to cell growth. We have previously obtained a global portrait of ion channel expression in contractile versus proliferating VSMCs in different vascular beds, in vitro and in vivo, and have identified a marked increase in Kv1.3 mRNA expression during the switch to a proliferative phenotype. The aim of our study is to investigate the effect of the selective blockade of Kv1.3 channels in VSMC proliferation. For this purpose, we have selected PAP-1 (phenoxyalkoxypsoralen-1), a potent suppressor of T cells proliferation in vitro, which inhibits Kv1.3 with a high selectivity over other K+ channels. [Methods]: Porcine coronary SMCs were isolated and cell proliferation analysis was measured with a BrdU incorporation assay. Using an arterial injury model previously validated by our group, an endothelial denudation injury was induced to murine femoral arteries. A constant infusion of PAP-1 (50 microg/Kg) was administered after injury, through the subcutaneous implant of Alzet osmotic mini-pumps, during 28 days, time-point at which animals were euthanized and arterial segments collected for morphometric and immunohistochemical analysis. [Results]: PAP-1 (10 nM) significantly reduced cell proliferation versus control cells (13,2±1% vs. 18±1%, p<0,05). Intimal proliferation was reduced in PAP-1-treated animals, compared with control, vehicle-treated, mice (Intima-to-media ratios of 0,18±0,11 vs. 1,06±0,40; p=0,01). [Conclusion]: The selective blockade of Kv1.3 channels decreases in vitro VSMCs proliferation and in vivo intimal hyperplasia formation. Our results point to Kv1.3 channels as a new promising therapeutical target to avoid restenosis. | es_ES |
dc.language.iso | eng | es_ES |
dc.rights | closedAccess | es_ES |
dc.title | Role of KV1.3 channels in intimal hyperlasia | es_ES |
dc.type | póster de congreso | es_ES |
dc.description.peerreviewed | Peer reviewed | es_ES |
dc.relation.csic | Sí | es_ES |
dc.type.coar | http://purl.org/coar/resource_type/c_6670 | es_ES |
item.grantfulltext | none | - |
item.fulltext | No Fulltext | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.languageiso639-1 | en | - |
item.cerifentitytype | Publications | - |
item.openairetype | póster de congreso | - |
Aparece en las colecciones: | (IBGM) Comunicaciones congresos |
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