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Authordc.contributor.authorAbrigo, Johanna 
Authordc.contributor.authorGonzález, Francisco 
Authordc.contributor.authorAguirre, Francisco 
Authordc.contributor.authorTacchi, Franco 
Authordc.contributor.authorGonzález, Andrea 
Authordc.contributor.authorMeza, María Paz 
Authordc.contributor.authorSimón, Felipe 
Authordc.contributor.authorCabrera, Daniel 
Authordc.contributor.authorArrese, Marco 
Authordc.contributor.authorKarpen, Saúl 
Authordc.contributor.authorCabello Verrugio, Claudio 
Cita de ítemdc.identifier.citationJ Cell Physiol. 2020;1–13es_ES
Abstractdc.description.abstractSkeletal muscle atrophy is characterized by the degradation of myofibrillar proteins, such as myosin heavy chain or troponin. An increase in the expression of two muscle-specific E3 ligases, atrogin-1 and MuRF-1, and oxidative stress are involved in muscle atrophy. Patients with chronic liver diseases (CLD) develop muscle wasting. Several bile acids increase in plasma during cholestatic CLD, among them, cholic acid (CA) and deoxycholic acid (DCA). The receptor for bile acids, TGR5, is expressed in healthy skeletal muscles. TGR5 is involved in the regulation of muscle differentiation and metabolic changes. In this paper, we evaluated the participation of DCA and CA in the generation of an atrophic condition in myotubes and isolated fibers from the muscle extracted from wild-type (WT) and TGR5-deficient (TGR5(-/-)) male mice. The results show that DCA and CA induce a decrease in diameter, and myosin heavy chain (MHC) protein levels, two typical atrophic features in C2C12 myotubes. We also observed similar results when INT-777 agonists activated the TGR5 receptor. To evaluate the participation of TGR5 in muscle atrophy induced by DCA and CA, we used a culture of muscle fiber isolated from WT and TGR5(-/-) mice. Our results show that DCA and CA decrease the fiber diameter and MHC protein levels, and there is an increase in atrogin-1, MuRF-1, and oxidative stress in WT fibers. The absence of TGR5 in fibers abolished all these effects induced by DCA and CA. Thus, we demonstrated that CS and deoxycholic acid induce skeletal muscle atrophy through TGR5 receptor.es_ES
Patrocinadordc.description.sponsorshipBASAL Grant CEDENNA AFB180001 Programa de Cooperacion Cientifica ECOS-CONICYT C16S02 Millennium Institute on Immunology and Immunotherapy P09-016-F Comision Nacional de Investigacion Cientifica y Tecnologica (CONICYT) 21161353 Nucleus of Ion ChannelsAssociated Diseases MiNICAD Comision Nacional de Investigacion Cientifica y Tecnologica (CONICYT) AFB170005 National Fund for Science and Technological Development Fondecyt 11171001 Fondecyt 1161288 Fondecyt 1161646es_ES
Type of licensedc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile*
Link to Licensedc.rights.uri*
Sourcedc.sourceJournal of Cellular Physiologyes_ES
Keywordsdc.subjectBile acidses_ES
Keywordsdc.subjectMuscle atrophyes_ES
Keywordsdc.subjectMuscle wastinges_ES
Keywordsdc.subjectTGR5 receptores_ES
Keywordsdc.subjectUbiquitin-proteasome systemes_ES
Títulodc.titleCholic acid and deoxycholic acid induce skeletal muscle atrophy through a mechanism dependent on TGR5 receptores_ES
Document typedc.typeArtículo de revistaes_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