Morphological aspects of neuromuscular junctions and gene expression of nicotinic acetylcholine receptors (nAChRs) in skeletal muscle of rats with heart failure

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dc.contributor.authorTome de Souza, Paula Aiello [UNESP]
dc.contributor.authorMatheus, Selma Maria Michelin [UNESP]
dc.contributor.authorCastan, Eduardo Paulino [UNESP]
dc.contributor.authorSalome Campos, Dijon Henrique [UNESP]
dc.contributor.authorCicogna, Antonio Carlos [UNESP]
dc.contributor.authorCarvalho, Robson Francisco [UNESP]
dc.contributor.authorDal-Pai-Silva, Maeli [UNESP]
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2014-05-20T13:52:19Z
dc.date.available2014-05-20T13:52:19Z
dc.date.issued2011-12-01
dc.description.abstractHF is syndrome initiated by a reduction in cardiac function and it is characterized by the activation of compensatory mechanisms. Muscular fatigue and dyspnoea are the more common symptoms in HF; these may be due in part to specific skeletal muscle myopathy characterized by reduced oxidative capacity, a shift from slow fatigue resistant type I to fast less fatigue resistant type II fibers and downregulation of myogenic regulatory factors (MRFs) gene expression that can regulate gene expression of nicotinic acetylcholine receptors (nAChRs). In chronic heart failure, skeletal muscle phenotypic changes could influence the maintenance of the neuromuscular junction morphology and nAChRs gene expression during this syndrome. Two groups of rats were studied: control (CT) and Heart Failure (HF), induced by a single intraperitoneal injection of monocrotaline (MCT). At the end of the experiment, HF was evaluated by clinical signs and animals were sacrificed. Soleus (SOL) muscles were removed and processed for morphological, morphometric and molecular NMJ analyses. Our major finding was an up-regulation in the gene expression of the alpha1 and epsilon subunits of nAChR and a spot pattern of nAChR in SOL skeletal muscle in this acute monocrotaline induced HF. Our results suggest a remodeling of nAChR alpha1 and epsilon subunit during heart failure and may provide valuable information for understanding the skeletal muscle myopathy that occurs during this syndrome.en
dc.description.affiliationUniv Estadual Paulista, Dept Morphol, Inst Biosci, BR-18618970 São Paulo, Brazil
dc.description.affiliationUniv Estadual Paulista, Dept Anat, Inst Biosci, BR-18618970 São Paulo, Brazil
dc.description.affiliationUniv Estadual Paulista, Dept Internal Med, BR-18618970 São Paulo, Brazil
dc.description.affiliationUnespUniv Estadual Paulista, Dept Morphol, Inst Biosci, BR-18618970 São Paulo, Brazil
dc.description.affiliationUnespUniv Estadual Paulista, Dept Anat, Inst Biosci, BR-18618970 São Paulo, Brazil
dc.description.affiliationUnespUniv Estadual Paulista, Dept Internal Med, BR-18618970 São Paulo, Brazil
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorshipIdCNPq: 00751/07DFP
dc.description.sponsorshipIdCNPq: 557-01-DCP
dc.format.extent557-565
dc.identifierhttp://dx.doi.org/10.1007/s10735-011-9354-2
dc.identifier.citationJournal of Molecular Histology. Dordrecht: Springer, v. 42, n. 6, p. 557-565, 2011.
dc.identifier.doi10.1007/s10735-011-9354-2
dc.identifier.issn1567-2379
dc.identifier.lattes5406518799128485
dc.identifier.lattes9418970103564137
dc.identifier.orcid0000-0002-4901-7714
dc.identifier.urihttp://hdl.handle.net/11449/18699
dc.identifier.wosWOS:000300371400008
dc.language.isoeng
dc.publisherSpringer
dc.relation.ispartofJournal of Molecular Histology
dc.relation.ispartofjcr2.412
dc.relation.ispartofsjr0,981
dc.rights.accessRightsAcesso restrito
dc.sourceWeb of Science
dc.subjectHeart failureen
dc.subjectNeuromuscular junctionen
dc.subjectSkeletal muscleen
dc.subjectNicotinic acetylcholine receptorsen
dc.subjectGene expressionen
dc.titleMorphological aspects of neuromuscular junctions and gene expression of nicotinic acetylcholine receptors (nAChRs) in skeletal muscle of rats with heart failureen
dc.typeArtigo
dcterms.licensehttp://www.springer.com/open+access/authors+rights?SGWID=0-176704-12-683201-0
dcterms.rightsHolderSpringer
unesp.author.lattes5406518799128485
unesp.author.lattes9418970103564137[5]
unesp.author.orcid0000-0002-4901-7714[6]
unesp.author.orcid0000-0002-4402-6523[5]
unesp.campusUniversidade Estadual Paulista (Unesp), Instituto de Biociências, Botucatupt
unesp.campusUniversidade Estadual Paulista (Unesp), Faculdade de Medicina, Botucatupt

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