Mitochondrial damage as death inducer in heart-derived H9c2 cells: more than one way for an early demise

Lax Pérez, Antonio Manuel; Fernandez Belda, Francisco; Soler Pardo, Fernando

Publication:
Mitochondrial damage as death inducer in heart-derived H9c2 cells: more than one way for an early demise

dc.contributor.author	Lax Pérez, Antonio Manuel
dc.contributor.author	Fernandez Belda, Francisco
dc.contributor.author	Soler Pardo, Fernando
dc.contributor.department	Medicina
dc.date.accessioned	2024-07-15T11:23:42Z
dc.date.available	2024-07-15T11:23:42Z
dc.date.issued	2009-09-24
dc.description	© 2009 Springer Science Business Media. This document is the Published version of a Published Work that appeared in final form in Journal of Bioenergetics and Biomembranes. To access the final edited and published work see https://doi.org/10.1007/s10863-009-9236-4
dc.description.abstract	The release of cytochrome c from mitochondria induced by 10 microM thapsigargin was linked to rapid loss of the mitochondrial membrane potential whereas that induced by 50 nM staurosporine was mediated by Bax activation and occurred in polarized mitochondria. Similar levels of cytochrome c were observed when induced by either thapsigargin or staurosporine indicating that the release magnitude was independent of the mechanism involved in membrane permeabilization. In any case caspase 3 activation was subsequent to cytochrome c release. Mitochondrial dysfunction and release of cytochrome c occurred earlier when induced by thapsigargin even though morphological alteration of the cell and chromatin condensation were developed earlier in the presence of staurosporine. In addition, a general and irreversible caspase inhibitor did not protect against chromatin condensation induced by staurosporine. It is also shown that earlier mitochondrial damage does not always correlate with earlier cell demise. This can be attributed to the existence of alternative caspase-independent cell death programmes.	es
dc.format	application/pdf	es
dc.format.extent	9	es
dc.identifier.citation	Journal of Bioenergetics and Biomembranes, 2009, Vol. 41, pp. 369–377
dc.identifier.doi	https://doi.org/10.1007/s10863-009-9236-4
dc.identifier.issn	Print: 0145-479X
dc.identifier.issn	Electronic: 1573-6881
dc.identifier.uri	http://hdl.handle.net/10201/143091
dc.language	eng	es
dc.publisher	Springer
dc.relation	This study was supported by grant BMC2002-02474 from Ministerio de Educación y Cultura, Spain and by a grant-in-aid from the Universidad de Murcia	es
dc.relation.publisherversion	https://link.springer.com/article/10.1007/s10863-009-9236-4#article-info
dc.rights.accessRights	info:eu-repo/semantics/restrictedAccess
dc.subject	Staurosporine	es
dc.subject	Thapsigargin	es
dc.subject	Mitochondria	es
dc.subject	Cell death	es
dc.subject	Cardiomyocyte	es
dc.subject.other	CDU::6 - Ciencias aplicadas	es
dc.title	Mitochondrial damage as death inducer in heart-derived H9c2 cells: more than one way for an early demise	es
dc.type	info:eu-repo/semantics/article	es
dspace.entity.type	Publication	es
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relation.isAuthorOfPublication.latestForDiscovery	fb419085-b327-4302-860b-d0f7e5000ea9