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Autordc.contributor.authorEisner, Verónica 
Autordc.contributor.authorCriollo Céspedes, Alfredo 
Autordc.contributor.authorQuiroga, Clara 
Autordc.contributor.authorOlea Azar, Claudio 
Autordc.contributor.authorSantibañez, Juan Francisco 
Autordc.contributor.authorTroncoso, Rodrigo 
Autordc.contributor.authorChiong Lay, Mario 
Autordc.contributor.authorDíaz Araya, Guillermo 
Autordc.contributor.authorFoncea, Rocío 
Autordc.contributor.authorLavandero González, Sergio 
Fecha ingresodc.date.accessioned2018-12-20T15:09:55Z
Fecha disponibledc.date.available2018-12-20T15:09:55Z
Fecha de publicacióndc.date.issued2006
Cita de ítemdc.identifier.citationFEBS Letters, Volumen 580, Issue 18, 2018, Pages 4495-4500
Identificadordc.identifier.issn00145793
Identificadordc.identifier.other10.1016/j.febslet.2006.07.029
Identificadordc.identifier.urihttps://repositorio.uchile.cl/handle/2250/158065
Resumendc.description.abstractWe have recently shown that hyperosmotic stress activates p65/RelB NFκB in cultured cardiomyocytes with dichotomic actions on caspase activation and cell death. It remains unexplored how NFκB is regulated in cultured rat cardiomyocytes exposed to hyperosmotic stress. We study here: (a) if hyperosmotic stress triggers reactive oxygen species (ROS) generation and in turn whether they regulate NFκB and (b) if insulin-like growth factor-1 (IGF-1) modulates ROS production and NFκB activation in hyperosmotically-stressed cardiomyocytes. The results showed that hyperosmotic stress generated ROS in cultured cardiac myocytes, in particular the hydroxyl and superoxide species, which were inhibited by N-acetylcysteine (NAC). Hyperosmotic stress-induced NFκB activation as determined by IκBα degradation and NFκB DNA binding. NFκB activation and procaspase-3 and -9 fragmentation were prevented by NAC and IGF-1. However, this growth factor did not decrease ROS generation induced by hyperosmotic stres
Idiomadc.language.isoen
Tipo de licenciadc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile
Link a Licenciadc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/
Fuentedc.sourceFEBS Letters
Palabras clavesdc.subjectCardiomyocyte
Palabras clavesdc.subjectCaspase
Palabras clavesdc.subjectHyperosmotic stress
Palabras clavesdc.subjectIGF-1
Palabras clavesdc.subjectNFκB
Palabras clavesdc.subjectReactive oxygen species
Títulodc.titleHyperosmotic stress-dependent NFκB activation is regulated by reactive oxygen species and IGF-1 in cultured cardiomyocytes
Tipo de documentodc.typeArtículo de revista
Catalogadoruchile.catalogadorSCOPUS
Indizaciónuchile.indexArtículo de publicación SCOPUS
uchile.cosechauchile.cosechaSI


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Attribution-NonCommercial-NoDerivs 3.0 Chile
Excepto si se señala otra cosa, la licencia del ítem se describe como Attribution-NonCommercial-NoDerivs 3.0 Chile