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Intracellular Ca2+ Pools and Fluxes in Cardiac Muscle-Derived H9c2 Cells

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dc.contributor.authorLax PĂ©rez, Antonio Manuel
dc.contributor.authorFernandez Belda, Francisco
dc.contributor.authorSoler Pardo, Fernando
dc.contributor.departmentMedicina
dc.date.accessioned2024-01-23T09:37:49Z
dc.date.available2024-01-23T09:37:49Z
dc.date.issued2005-08
dc.description©2005. 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 Journal of Bioenergetics and Biomembranes. To access the final edited and published work see https://doi.org/ 10.1007/s10863-005-6635-zes
dc.description.abstractRelevant Ca(2+) pools and fluxes in H9c2 cells have been studied using fluorescent indicators and Ca(2+)-mobilizing agents. Vasopressin produced a cytoplasmic Ca(2+) peak with half-maximal effective concentration of 6 nM, whereas thapsigargin-induced Ca(2+) increase showed half-maximal effect at 3 nM. Depolarization of the mitochondrial inner membrane by protonophore was also associated with an increase in cytoplasmic Ca(2+). Ionomycin induced a small and sustained depolarization, while thapsigargin had a small but transient effect. The thapsigargin-sensitive Ca(2+) pool was also sensitive to ionomycin, whereas the protonophore-sensitive Ca(2+) pool was not. The vasopressin-induced cytoplasmic Ca(2+) signal, which caused a reversible discharge of the sarco-endoplasmic reticulum Ca(2+) pool, was sensed as a mitochondrial Ca(2+) peak but was unaffected by the permeability transition pore inhibitor cyclosporin A. The mitochondrial Ca(2+) peak was affected by cyclosporin A when the Ca(2+) signal was induced by irreversible discharge of the intracellular Ca(2+) pool, i.e., adding thapsigargin. These observations indicate that the mitochondria interpret the cytoplasmic Ca(2+) signals generated in the reticular store.es
dc.formatapplication/pdfes
dc.format.extent11es
dc.identifier.citationJournal of Bioenergetics and Biomembranes 2005 Aug 37(4):249-59.doi: 10.1007/s10863-005-6635-z.
dc.identifier.doi10.1007/s10863-005-6635-z
dc.identifier.issn1573-6881
dc.identifier.issn0145-479X
dc.identifier.urihttp://hdl.handle.net/10201/137584
dc.languageenges
dc.relationThis study was supported by grants BMC2002-02474 from the Spanish Ministerio de Ciencia y Tecnolog´ıa/Fondo Europeo de Desarrollo Regional and PI-22/00756/FS/01 from Fundaci´on S´eneca de la Comunidad Aut´onoma de Murcia, Spain.es
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+ poolses
dc.subjectThapsigargines
dc.subjectVasopressines
dc.subjectSarco-endoplasmic reticulumes
dc.subjectCytoplasmic Ca2+es
dc.subjectMitochondrial Ca2+es
dc.subjectCardiomyocytees
dc.subject.otherCDU::6 - Ciencias aplicadases
dc.titleIntracellular Ca2+ Pools and Fluxes in Cardiac Muscle-Derived H9c2 Cellses
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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