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dc.contributor.authorCisterna, Bruno A.
dc.contributor.authorVargas, Aníbal A.
dc.contributor.authorPuebla, Carlos
dc.contributor.authorFernández, Paola
dc.contributor.authorEscamilla, Rosalba
dc.contributor.authorLagos, Carlos F.
dc.contributor.authorMatus, María F.
dc.contributor.authorVilos, Cristian
dc.contributor.authorCea, Luis A.
dc.contributor.authorBarnafi, Esteban
dc.contributor.authorGaete, Hugo
dc.contributor.authorEscobar, Daniel F.
dc.contributor.authorCardozo, Christopher P.
dc.contributor.authorSáez, Juan C.
dc.date.accessioned2020-03-04T11:27:02Z
dc.date.available2020-03-04T11:27:02Z
dc.date.issued2020
dc.identifier.citationCisterna, B. A., Vargas, A. A., Puebla, C., Fernández, P., Escamilla, R., Lagos, C. F., Matus, M. F., Vilos, C., Cea, L. A., Barnafi, E., Gaete, H., Escobar, D. F., Cardozo, C. P., & Sáez, J. C. (2020). Active acetylcholine receptors prevent the atrophy of skeletal muscles and favor reinnervation. <i>Nature Communications</i>, <i>11</i>, Article 1073. <a href="https://doi.org/10.1038/s41467-019-14063-8" target="_blank">https://doi.org/10.1038/s41467-019-14063-8</a>
dc.identifier.otherCONVID_34905373
dc.identifier.urihttps://jyx.jyu.fi/handle/123456789/68059
dc.description.abstractDenervation of skeletal muscles induces severe muscle atrophy, which is preceded by cellular alterations such as increased plasma membrane permeability, reduced resting membrane potential and accelerated protein catabolism. The factors that induce these changes remain unknown. Conversely, functional recovery following denervation depends on successful reinnervation. Here, we show that activation of nicotinic acetylcholine receptors (nAChRs) by quantal release of acetylcholine (ACh) from motoneurons is sufficient to prevent changes induced by denervation. Using in vitro assays, ACh and non-hydrolysable ACh analogs repressed the expression of connexin43 and connexin45 hemichannels, which promote muscle atrophy. In co-culture studies, connexin43/45 hemichannel knockout or knockdown increased innervation of muscle fibers by dorsal root ganglion neurons. Our results show that ACh released by motoneurons exerts a hitherto unknown function independent of myofiber contraction. nAChRs and connexin hemichannels are potential molecular targets for therapeutic intervention in a variety of pathological conditions with reduced synaptic neuromuscular transmission.en
dc.format.mimetypeapplication/pdf
dc.languageeng
dc.language.isoeng
dc.publisherNature Publishing Group
dc.relation.ispartofseriesNature Communications
dc.rightsCC BY 4.0
dc.subject.otherskeletal muscle
dc.subject.othersomatic system
dc.titleActive acetylcholine receptors prevent the atrophy of skeletal muscles and favor reinnervation
dc.typearticle
dc.identifier.urnURN:NBN:fi:jyu-202003042281
dc.contributor.laitosFysiikan laitosfi
dc.contributor.laitosDepartment of Physicsen
dc.contributor.oppiaineNanoscience Centerfi
dc.contributor.oppiaineNanoscience Centeren
dc.type.urihttp://purl.org/eprint/type/JournalArticle
dc.description.reviewstatuspeerReviewed
dc.relation.issn2041-1723
dc.relation.volume11
dc.type.versionpublishedVersion
dc.rights.copyright© The Authors 2020
dc.rights.accesslevelopenAccessfi
dc.subject.ysohermosolut
dc.subject.ysovälittäjäaineet
dc.subject.ysolihassurkastumasairaudet
dc.subject.ysoasetyylikoliini
dc.subject.ysosoluviestintä
dc.subject.ysolihakset
dc.format.contentfulltext
jyx.subject.urihttp://www.yso.fi/onto/yso/p18309
jyx.subject.urihttp://www.yso.fi/onto/yso/p22948
jyx.subject.urihttp://www.yso.fi/onto/yso/p15977
jyx.subject.urihttp://www.yso.fi/onto/yso/p323
jyx.subject.urihttp://www.yso.fi/onto/yso/p28740
jyx.subject.urihttp://www.yso.fi/onto/yso/p2784
dc.rights.urlhttps://creativecommons.org/licenses/by/4.0/
dc.relation.doi10.1038/s41467-019-14063-8
jyx.fundinginformationJ.C.S. acknowledges support from Fondo Nacional de Desarrollo Científico y Tecnológico (FONDECYT) grants 1111033, 1191329, and ICM-Economía grant P09-022-F from ICM-ECONOMIA, Chile. B.A.C. thanks FONDECYT grant 3170938 and CINV. C.V. acknowledges support from FONDECYT grant 11614338, BASAL Grant FB0807, and H2020-MSCA-RISE-2016 grant 734801 MAGNAMED. C.C. acknowledges support from the Department of Veterans Affairs, Rehabilitation Research and Development Service grant B-2020-C.


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