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Connexin-and pannexin-based channels in normal skeletal muscles and their possible role in muscle atrophy

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Autor dc.contributor.author Cea L.A.
Autor dc.contributor.author Riquelme M.A.
Autor dc.contributor.author Cisterna B.A.
Autor dc.contributor.author Puebla C.
Autor dc.contributor.author Vega J.L.
Autor dc.contributor.author Rovegno M.
Autor dc.contributor.author Saez J.C.
Fecha Ingreso dc.date.accessioned 2014-04-05T00:15:42Z
Fecha Disponible dc.date.available 2014-04-05T00:15:42Z
Fecha en Repositorio dc.date.issued 2014-04-04
dc.identifier 10.1007/s00232-012-9485-8
dc.description.abstract Precursor cells of skeletal muscles express connexins 39, 43 and 45 and pannexin1. In these cells, most connexins form two types of membrane channels, gap junction channels and hemichannels, whereas pannexin1 forms only hemichannels. All these channels are low-resistance pathways permeable to ions and small molecules that coordinate developmental events. During late stages of skeletal muscle differentiation, myofibers become innervated and stop expressing connexins but still express pannexin1 hemichannels that are potential pathways for the ATP release required for potentiation of the contraction response. Adult injured muscles undergo regeneration, and connexins are reexpressed and form membrane channels. In vivo, connexin reexpression occurs in undifferentiated cells that form new myofibers, favoring the healing process of injured muscle. However, differentiated myofibers maintained in culture for 48 h or treated with proinflammatory cytokines for less than 3 h also reexpress connexins and only form functional hemichannels at the cell surface. We propose that opening of these hemichannels contributes to drastic changes in electrochemical gradients, including reduction of membrane potential, increases in intracellular free Ca2+ concentration and release of diverse metabolites (e.g., NAD + and ATP) to the extracellular milieu, contributing to multiple metabolic and physiologic alterations that characterize muscles undergoing atrophy in several acquired and genetic human diseases. Consequently, inhibition of connexin hemichannels expressed by injured or denervated skeletal muscles might reduce or prevent deleterious changes triggered by conditions that promote muscle atrophy. © Springer Science+Business Media, LLC 2012. en_US
dc.source Journal of Membrane Biology
Link Descarga dc.source.uri http://www.scopus.com/inward/record.url?eid=2-s2.0-84866738493&partnerID=40&md5=1fbaa0f97b043580608e71576f393147
Title dc.title Connexin-and pannexin-based channels in normal skeletal muscles and their possible role in muscle atrophy en_US
Tipo dc.type Review
dc.description.keywords adenosine triphosphate; cytokine; gap junction protein; membrane protein; pannexin; unclassified drug; calcium cell level; human; ion permeability; membrane potential; molecular library; muscle atrophy; muscle development; muscle injury; muscle regeneration; myoblast; myopathy; ontogeny; protein expression; review; skeletal muscle; Animals; Connexins; Humans; Ion Channel Gating; Models, Biological; Muscle, Skeletal; Muscular Atrophy; Nerve Tissue Proteins; Reference Values en_US


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