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Hyperosmotic stress-dependent NFκB activation is regulated by reactive oxygen species and IGF-1 in cultured cardiomyocytes
Autor | dc.contributor.author | Eisner, Verónica | |
Autor | dc.contributor.author | Criollo Céspedes, Alfredo | |
Autor | dc.contributor.author | Quiroga, Clara | |
Autor | dc.contributor.author | Olea Azar, Claudio | |
Autor | dc.contributor.author | Santibañez, Juan Francisco | |
Autor | dc.contributor.author | Troncoso, Rodrigo | |
Autor | dc.contributor.author | Chiong Lay, Mario | |
Autor | dc.contributor.author | Díaz Araya, Guillermo | |
Autor | dc.contributor.author | Foncea, Rocío | |
Autor | dc.contributor.author | Lavandero González, Sergio | |
Fecha ingreso | dc.date.accessioned | 2018-12-20T15:09:55Z | |
Fecha disponible | dc.date.available | 2018-12-20T15:09:55Z | |
Fecha de publicación | dc.date.issued | 2006 | |
Cita de ítem | dc.identifier.citation | FEBS Letters, Volumen 580, Issue 18, 2018, Pages 4495-4500 | |
Identificador | dc.identifier.issn | 00145793 | |
Identificador | dc.identifier.other | 10.1016/j.febslet.2006.07.029 | |
Identificador | dc.identifier.uri | https://repositorio.uchile.cl/handle/2250/158065 | |
Resumen | dc.description.abstract | We 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 | |
Idioma | dc.language.iso | en | |
Tipo de licencia | dc.rights | Attribution-NonCommercial-NoDerivs 3.0 Chile | |
Link a Licencia | dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/3.0/cl/ | |
Fuente | dc.source | FEBS Letters | |
Palabras claves | dc.subject | Cardiomyocyte | |
Palabras claves | dc.subject | Caspase | |
Palabras claves | dc.subject | Hyperosmotic stress | |
Palabras claves | dc.subject | IGF-1 | |
Palabras claves | dc.subject | NFκB | |
Palabras claves | dc.subject | Reactive oxygen species | |
Título | dc.title | Hyperosmotic stress-dependent NFκB activation is regulated by reactive oxygen species and IGF-1 in cultured cardiomyocytes | |
Tipo de documento | dc.type | Artículo de revista | |
Catalogador | uchile.catalogador | SCOPUS | |
Indización | uchile.index | Artículo de publicación SCOPUS | |
uchile.cosecha | uchile.cosecha | SI |
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