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dc.contributor.authorMuñoz, Eva-
dc.contributor.authorSobradillo, Diego-
dc.contributor.authorHernández-Morales, Miriam-
dc.contributor.authorRocher, Asunción-
dc.contributor.authorNúñez, Lucía-
dc.contributor.authorVillalobos, Carlos-
dc.date.accessioned2015-06-25T12:46:18Z-
dc.date.available2015-06-25T12:46:18Z-
dc.date.issued2012-
dc.identifier.citationJoint FEPS-SECF Meeting 2012-
dc.identifier.urihttp://hdl.handle.net/10261/117185-
dc.descriptionResumen del trabajo presentado al Joint FEPS & XXXVI Spanish Physiological Society Congress (Sociedad Española de Ciencias Fisiológicas) celebrado en Santiago de Compostela (España) del 8 al 11 de septiembre de 2012.-
dc.description.abstract[Objectives]: Abnormal proliferation of vascular smooth muscle cells, a process related to ion channel remodeling, contribute to occlusive disorders including restenosis and atherosclerosis. Nonsteroidal anti-inflammatory drugs (NSAIDs) prevent VSMC proliferation and occlusive disorders by an unknown mechanism. We aimed at characterizing the role of calcium channel remodeling in the reversal phenotypic switch of cultured human coronary artery smooth muscle cells (hCASMCs) and the antiproliferative mechanism of NSAIDs. [Materials]: For this end we used cytosolic and mitochondrial calcium imaging and electrophysiological recordings in addition to real-time PCR and western blotting. [Results]: We found that early passage hCASMCs showed a proliferating phenotype, proliferation depending fully on store-operated calcium entry (SOCE), but not on voltage-operated calcium entry (VOCE). Proliferating hCASMCs showed large SOCE, SOCE-induced mitochondrial calcium uptake and Stim1 whereas VOCE was residual. NSAIDs inhibited SOCE as well as proliferation and migration. After a few passages hCASM cells switched to a non proliferating phenotype characterized by decreased SOCE and Stim1 and increased VOCE, Cav1.2 and VOCE-induced mitochondrial calcium uptake. NSAIDs failed to inhibit SOCE in the non-proliferating cells. [Conclusions]: We conclude that proliferating hCASMCs undergo a reversal phenotypic switch in culture towards quiescent cells mediated by remodeling of calcium channels that may reflect the changes underlying vascular occlusive disorders. NSAIDs inhibit SOCE and hCASMC proliferation and migration in a mitochondria-dependent, phenotypic specific manner.-
dc.description.sponsorshipThis work was funded by DIGICYT (BFU2009-08967) and Junta de Castilla y León, Spain (VA270A11-2). EM and DS were supported by predoctoral fellowships from FPI (DIGICYT) and JAE (CSI) programs, respectively.-
dc.rightsclosedAccess-
dc.titleRole of calcium channel remodeling in the reversal phenotypic switch of human coronary artery smooth muscle cells, and the effects of NSAIDs-
dc.typecomunicación de congreso-
dc.date.updated2015-06-25T12:46:19Z-
dc.description.versionPeer Reviewed-
dc.language.rfc3066eng-
dc.contributor.funderJunta de Castilla y León-
dc.contributor.funderDirección General de Investigación Científica y Técnica, DGICT (España)-
dc.contributor.funderConsejo Superior de Investigaciones Científicas (España)-
dc.relation.csic-
dc.identifier.funderhttp://dx.doi.org/10.13039/501100003339es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100008737es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100014180es_ES
dc.type.coarhttp://purl.org/coar/resource_type/c_5794es_ES
item.openairetypecomunicación de congreso-
item.cerifentitytypePublications-
item.grantfulltextnone-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextNo Fulltext-
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