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Cellular death linked to irreversible stress in the sarcoplasmic reticulum: the effect of inhibiting Ca(2+) -ATPase or protein glycosylation in the myocardiac cell model H9c2

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dc.contributor.authorLax Pérez, Antonio Manuel
dc.contributor.authorFernandez Belda, Francisco
dc.contributor.authorSoler Pardo, Fernando
dc.contributor.departmentMedicina
dc.date.accessioned2024-01-23T09:55:14Z
dc.date.available2024-01-23T09:55:14Z
dc.date.issued2007-10
dc.description©2007. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/ This document is the Accepted version of a Published Work that appeared in final form in Archives of Biochemistry and Biophysics. To access the final edited and published work see https://doi.org/10.1016/j.abb.2007.06.022es
dc.description.abstractExperimental sarcoplasmic reticulum damage induced by 3 microM thapsigargin or 1 microg/ml tunicamycin provoked viability loss of the cell population in approximately 72 h. Release of cytochrome c from mitochondria was an early event and Bax translocation to the mitochondria preceded or was simultaneous with cytochrome c release. The release of cytochrome c was not related with mitochondria depolarization or caspase activation. Irreversible stress in the sarcoplasmic reticulum, detected by the early activation of caspase 12, was functionally linked to the mitochondrial apoptotic pathway. Caspase 3 processing was blocked by cells preincubation with a selective inhibitor of either caspase 9 or caspase 8 whereas caspase 8 activation was inhibited by a selective caspase 9 inhibitor. This was consistent with the involvement of caspase 8 in a positive feedback loop leading to amplify the caspase cascade. Caspase inhibition did not protect against cell death indicating the existence of alternative caspase-independent mechanisms.es
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dc.format.extent9es
dc.identifier.citationArchives of Biochemistry and Biophysics. 2007 Oct 15 466(2):194-202.doi: 10.1016/j.abb.2007.06.022.
dc.identifier.doi10.1016/j.abb.2007.06.022
dc.identifier.issn1096-0384
dc.identifier.issn0003-9861
dc.identifier.urihttp://hdl.handle.net/10201/137587
dc.languageenges
dc.relationThis study was funded by Grant BCM2002-02474 from the Spanish Ministerio de Educacio´n y Ciencia/ Fondo Europeo de Desarrollo Regional and by a grant-in-aid from the Universidad de Murciaes
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectCa2+–ATPase inhibitiones
dc.subjectThapsigargin; Tunicamycines
dc.subjectSarcoplasmic reticulumes
dc.subjectCell deathes
dc.subjectCardiac cell linees
dc.titleCellular death linked to irreversible stress in the sarcoplasmic reticulum: the effect of inhibiting Ca(2+) -ATPase or protein glycosylation in the myocardiac cell model H9c2es
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
relation.isAuthorOfPublicationfb419085-b327-4302-860b-d0f7e5000ea9
relation.isAuthorOfPublication.latestForDiscoveryfb419085-b327-4302-860b-d0f7e5000ea9
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