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Mitochondrial calcium increase induced by RyR1 and IP3R channel activation after membrane depolarization regulates skeletal muscle metabolism

Autordc.contributor.authorDíaz Vegas, Alexis 
Autordc.contributor.authorCórdova, A. 
Autordc.contributor.authorValladares, Denisse 
Autordc.contributor.authorLlanos, Paola 
Autordc.contributor.authorHidalgo, C. 
Autordc.contributor.authorGherardi, Gaia 
Autordc.contributor.authorStefani, Diego De 
Autordc.contributor.authorMammucari, Cristina 
Autordc.contributor.authorRizzuto, Rosario 
Autordc.contributor.authorContreras Ferrat, Ariel 
Autordc.contributor.authorJaimovich Pérez, Enrique 
Fecha ingresodc.date.accessioned2018-11-08T20:30:43Z
Fecha disponibledc.date.available2018-11-08T20:30:43Z
Fecha de publicacióndc.date.issued2018-06
Cita de ítemdc.identifier.citationFrontiers in Physiology Volumen: 9 Número de artículo: 791es_ES
Identificadordc.identifier.other10.3389/fphys.2018.00791
Identificadordc.identifier.urihttp://repositorio.uchile.cl/handle/2250/152524
Resumendc.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
Idiomadc.language.isoenes_ES
Publicadordc.publisherFrontiers Mediaes_ES
Tipo de licenciadc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile*
Link a Licenciadc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/*
Fuentedc.sourceFrontiers in Physiologyes_ES
Palabras clavesdc.subjectEnergy distributiones_ES
Palabras clavesdc.subjectInositol 1, 4, 5-trisphosphate receptores_ES
Palabras clavesdc.subjectMitochondria heterogeneityes_ES
Palabras clavesdc.subjectMitochondrial networkes_ES
Palabras clavesdc.subjectRyanodine receptorses_ES
Títulodc.titleMitochondrial calcium increase induced by RyR1 and IP3R channel activation after membrane depolarization regulates skeletal muscle metabolismes_ES
Tipo de documentodc.typeArtículo de revistaes_ES
Catalogadoruchile.catalogadorrgfes_ES
Indizaciónuchile.indexArtículo de publicación ISIes_ES


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Attribution-NonCommercial-NoDerivs 3.0 Chile
Excepto si se señala otra cosa, la licencia del ítem se describe como Attribution-NonCommercial-NoDerivs 3.0 Chile