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Authordc.contributor.authorDíaz Vegas, Alexis 
Authordc.contributor.authorCórdova, A. 
Authordc.contributor.authorValladares, Denisse 
Authordc.contributor.authorLlanos Vidal, Paola 
Authordc.contributor.authorHidalgo, C. 
Authordc.contributor.authorGherardi, Gaia 
Authordc.contributor.authorStefani, Diego De 
Authordc.contributor.authorMammucari, Cristina 
Authordc.contributor.authorRizzuto, Rosario 
Authordc.contributor.authorContreras Ferrat, Ariel Eduardo 
Authordc.contributor.authorJaimovich Pérez, Enrique 
Admission datedc.date.accessioned2018-11-08T20:30:43Z
Available datedc.date.available2018-11-08T20:30:43Z
Publication datedc.date.issued2018-06
Cita de ítemdc.identifier.citationFrontiers in Physiology Volumen: 9 Número de artículo: 791es_ES
Identifierdc.identifier.other10.3389/fphys.2018.00791
Identifierdc.identifier.urihttps://repositorio.uchile.cl/handle/2250/152524
Abstractdc.description.abstractAim: We hypothesize that both type-1 ryanodine receptor (RyR1) and IP3-receptor (IP3R) calcium channels are necessary for the mitochondrial Ca2+ increase caused by membrane depolarization induced by potassium (or by electrical stimulation) of single skeletal muscle fibers; this calcium increase would couple muscle fiber excitation to an increase in metabolic output from mitochondria (excitation-metabolism coupling). Methods: Mitochondria matrix and cytoplasmic Ca2+ levels were evaluated in fibers isolated from flexor digitorium brevis muscle using plasmids for the expression of a mitochondrial Ca2+ sensor (CEPIA3mt) or a cytoplasmic Ca2+ sensor (RCaMP). The role of intracellular Ca2+ channels was evaluated using both specific pharmacological inhibitors (xestospongin B for IP3R and Dantrolene for RyR1) and a genetic approach (shIP(3)R1-RFP). O-2 consumption was detected using Seahorse Extracellular Flux Analyzer. Results: In isolated muscle fibers cell membrane depolarization increased both cytoplasmic and mitochondrial Ca2+ levels. Mitochondrial C-a2+ uptake required functional inositol IP3R and RyR1 channels. Inhibition of either channel decreased basal O-2 consumption rate but only RyR1 inhibition decreased ATP-linked O-2 consumption. Cell membrane depolarization-induced Ca2+ signals in sub-sarcolemmal mitochondria were accompanied by a reduction in mitochondrial membrane potential; Ca2+ signals propagated toward intermyofibrillar mitochondria, which displayed increased membrane potential. These results are compatible with slow, Ca2+-dependent propagation of mitochondrial membrane potential from the surface toward the center of the fiber. Conclusion: Ca2+-dependent changes in mitochondrial membrane potential have different kinetics in the surface vs. the center of the fiber; these differences are likely to play a critical role in the control of mitochondrial metabolism, both at rest and after membrane depolarization as part of an excitation-metabolism coupling process in skeletal muscle fibers.es_ES
Patrocinadordc.description.sponsorshipFONDECYT 1151293 AT 21150604 11150243 BNI-09-15-F 11130267es_ES
Lenguagedc.language.isoenes_ES
Publisherdc.publisherFrontiers Mediaes_ES
Type of licensedc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile*
Link to Licensedc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/*
Sourcedc.sourceFrontiers in Physiologyes_ES
Keywordsdc.subjectEnergy distributiones_ES
Keywordsdc.subjectInositol 1, 4, 5-trisphosphate receptores_ES
Keywordsdc.subjectMitochondria heterogeneityes_ES
Keywordsdc.subjectMitochondrial networkes_ES
Keywordsdc.subjectRyanodine receptorses_ES
Títulodc.titleMitochondrial calcium increase induced by RyR1 and IP3R channel activation after membrane depolarization regulates skeletal muscle metabolismes_ES
Document typedc.typeArtículo de revista
Catalogueruchile.catalogadorrgfes_ES
Indexationuchile.indexArtículo de publicación ISIes_ES


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Attribution-NonCommercial-NoDerivs 3.0 Chile
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-NoDerivs 3.0 Chile