Hyperosmotic stress-dependent NFκB activation is regulated by reactive oxygen species and IGF-1 in cultured cardiomyocytes

Simple item page
dc.contributor.authorEisner, Veronica
dc.contributor.authorCriollo, Alfredo
dc.contributor.authorQuiroga, Clara
dc.contributor.authorOlea-Azar, Claudio
dc.contributor.authorSantibanez, Juan Francisco
dc.contributor.authorTroncoso, Rodrigo
dc.contributor.authorChiong, Mario
dc.contributor.authorDiaz-Araya, Guillermo
dc.contributor.authorFoncea, Rocio
dc.contributor.authorLavandero, Sergio
dc.date.accessioned2025-01-21T01:06:00Z
dc.date.available2025-01-21T01:06:00Z
dc.date.issued2006
dc.description.abstractWe have recently shown that hyperosmotic stress activates p65/RelB NF kappa B in cultured cardiomyocytes with dichotomic actions on caspase activation and cell death. It remains unexplored how NFKB 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 NFKB and (b) if insulin-like growth factor-1 (IGF-1) modulates ROS production and NF kappa B 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 NFKB activation as determined by I kappa B alpha degradation and NF kappa B DNA binding. NFKB 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 stress, suggesting that its actions over NFKB and caspase activation may be due to modulation of events downstream of ROS generation. We conclude that hyperosmotic stress induces ROS, which in turn activates NF kappa B and caspases. IGF-1 prevents NFKB activation by a ROS-independent mechanism. (c) 2006 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
dc.fuente.origenWOS
dc.identifier.doi10.1016/j.febslet.2006.07.029
dc.identifier.issn0014-5793
dc.identifier.urihttps://doi.org/10.1016/j.febslet.2006.07.029
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/96066
dc.identifier.wosidWOS:000239669000032
dc.issue.numero18
dc.language.isoen
dc.pagina.final4500
dc.pagina.inicio4495
dc.revistaFebs letters
dc.rightsacceso restringido
dc.subjectIGF-1
dc.subjectNF kappa B
dc.subjecthyperosmotic stress
dc.subjectreactive oxygen species
dc.subjectcaspase
dc.subjectcardiomyocyte
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleHyperosmotic stress-dependent NFκB activation is regulated by reactive oxygen species and IGF-1 in cultured cardiomyocytes
dc.typeartículo
dc.volumen580
sipa.indexWOS
sipa.trazabilidadWOS;2025-01-12
Files
Collections
Artículos de revistas