dc.creatorBustamante, Mario
dc.creatorFernández Verdejo, Rodrigo
dc.creatorJaimovich Pérez, Enrique
dc.creatorBuvinic, Sonja
dc.date.accessioned2019-03-15T16:06:35Z
dc.date.available2019-03-15T16:06:35Z
dc.date.created2019-03-15T16:06:35Z
dc.date.issued2014
dc.identifierAmerican Journal of Physiology - Endocrinology and Metabolism, Volumen 306, Issue 8, 2018,
dc.identifier15221555
dc.identifier01931849
dc.identifier10.1152/ajpendo.00450.2013
dc.identifierhttps://repositorio.uchile.cl/handle/2250/166159
dc.description.abstractInterleukin-6 (IL-6) is an important myokine that is highly expressed in skeletal muscle cells upon exercise. We assessed IL-6 expression in response to electrical stimulation (ES) or extracellular ATP as a known mediator of the excitation-transcription mechanism in skeletal muscle. We examined whether the canonical signaling cascade downstream of IL-6 (IL-6/JAK2/STAT3) also responds to muscle cell excitation, concluding that IL-6 influences its own expression through a positive loop. Either ES or exogenous ATP (100 μM) increased both IL-6 expression and p-STAT3 levels in rat myotubes, a process inhibited by 100 μM suramin and 2 U/ml apyrase. ATP also evoked IL-6 expression in both isolated skeletal fibers and extracts derived from whole FDB muscles. ATP increased IL-6 release up to 10-fold. STAT3 activation evoked by ATP was abolished by the JAK2 inhibitor HBC. Blockade of secreted IL-6 with a neutralizing antibody or preincubation with the STAT3 inhibitor VIII reduced STAT3 activatio
dc.languageen
dc.publisherAmerican Physiological Society
dc.rightshttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/
dc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile
dc.sourceAmerican Journal of Physiology - Endocrinology and Metabolism
dc.subjectExercise
dc.subjectMuscle plasticity
dc.subjectMyokines
dc.subjectPurinergic signaling
dc.subjectSignal transducer and activator of transcription 3
dc.titleElectrical stimulation induces IL-6 in skeletal muscle through extracellular ATP by activating Ca2+ signals and an IL-6 autocrine loop
dc.typeArtículos de revistas


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