Heart Failure-Induced Diaphragm Myopathy

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dc.contributor.authorRuiz Lima, Aline Regina [UNESP]
dc.contributor.authorMartinez, Paula Felippe
dc.contributor.authorDamatto, Ricardo Luiz [UNESP]
dc.contributor.authorMariano Cezar, Marcelo Diarcadia [UNESP]
dc.contributor.authorGuizoni, Daniele Mendes [UNESP]
dc.contributor.authorBonomo, Camila [UNESP]
dc.contributor.authorOliveira, Silvio Assis
dc.contributor.authorSilva, Maeli Dal-Pai [UNESP]
dc.contributor.authorZornoff, Leonardo Antonio Mamede [UNESP]
dc.contributor.authorOkoshi, Katashi [UNESP]
dc.contributor.authorOkoshi, Marina Politi [UNESP]
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.contributor.institutionUniversidade Federal de Mato Grosso do Sul (UFMS)
dc.date.accessioned2015-03-18T15:55:39Z
dc.date.available2015-03-18T15:55:39Z
dc.date.issued2014-01-01
dc.description.abstractBackground: Intracellular signaling pathways involved in skeletal myosin heavy chain (MyHC) isofornn alterations during heart failure (HF) are not completely understood. We tested the hypothesis that diaphragm expression of mitogen-activated protein kinases (MAPK) and myogenic regulatory factors is changed in rats with myocardial infarction (MI) induced HF. Methods: Six months after MI rats were subjected to transthoracic echocardiography. After euthanasia, infarcted rats were subdivided in MI/HF- group (with no HF evidence; n=10), and MI/HF+ (with right ventricular hypertrophy and lung congestion; n=10). Sham operated rats were used as controls (n=10). MyHC isofornns were analyzed by electrophoresis. Statistical analysis: ANOVA and Pearson correlation. Results: MI/HF- had left cardiac chambers dilation with systolic and diastolic left ventricular dysfunction. Cardiac injury was more intense in MI/HF+ than MI/HF-. MyHC I isoform percentage was higher in MI/HF+ than MI/HF-, and IIb isoform lower in MI/HF+ than Sham. Left atrial diameter-to-body weight ratio positively correlated with MyHC I (p=0.005) and negatively correlated with MyHC IIb (p=0.02). TNF-alpha serum concentration positively correlated with MyHC I isoform. Total and phosphorylated ERK was lower in MI/HF- and MI/HF+ than Sham. Phosphorylated JNK was lower in MI/HF- than Sham. JNK and p38 did not differ between groups. Expression of NF-kappa B and the myogenic regulatory factors MyoD, myogenin, and MRF4 was similar between groups. Conclusion: Diaphragm MyHC fast-to-slow shift is related to cardiac dysfunction severity and TNF-alpha serum levels in infarcted rats. Reduced ERK expression seems to participate in MyHC isofornn changes. Myogenic regulatory factors and NF-kappa B do not modulate diaphragm MyHC distribution during chronic HF. Copyright (C) 2014 S. Karger AG, Baselen
dc.description.affiliationUNESP, Botucatu Med Sch, Dept Internal Med, Botocutu, SP, Brazil
dc.description.affiliationFed Univ Mato Grosso Do Sul UFMS, Biol Sci & Hlth Ctr, Campo Grande, MS, Brazil
dc.description.affiliationUNESP, Biosci Inst, Dept Morphol, Botucatu, SP, Brazil
dc.description.affiliationUnespUNESP, Botucatu Med Sch, Dept Internal Med, Botocutu, SP, Brazil
dc.description.affiliationUnespUNESP, Biosci Inst, Dept Morphol, Botucatu, SP, Brazil
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipIdCNPq: 306857/2012-0
dc.description.sponsorshipIdCNPq: 306845/2012-1
dc.description.sponsorshipIdFAPESP: 07/57499-6
dc.description.sponsorshipIdFAPESP: 10/50084-8
dc.description.sponsorshipIdFAPESP: 08/58655-4
dc.format.extent333-345
dc.identifierhttp://dx.doi.org/10.1159/000363003
dc.identifier.citationCellular Physiology And Biochemistry. Basel: Karger, v. 34, n. 2, p. 333-345, 2014.
dc.identifier.doi10.1159/000363003
dc.identifier.fileWOS000343764600010.pdf
dc.identifier.issn1015-8987
dc.identifier.lattes1590971576309420
dc.identifier.lattes4463138671998432
dc.identifier.lattes5016839015394547
dc.identifier.urihttp://hdl.handle.net/11449/117256
dc.identifier.wosWOS:000343764600010
dc.language.isoeng
dc.publisherKarger
dc.relation.ispartofCellular Physiology And Biochemistry
dc.relation.ispartofjcr5.500
dc.relation.ispartofsjr1,561
dc.rights.accessRightsAcesso aberto
dc.sourceWeb of Science
dc.subjectSkeletal muscleen
dc.subjectMAPKen
dc.subjectMyogenic regulatory factorsen
dc.subjectMyosin heavy chain isoformsen
dc.subjectEchocardiographyen
dc.subjectMyocardial infarctionen
dc.titleHeart Failure-Induced Diaphragm Myopathyen
dc.typeArtigo
dcterms.licensehttp://www.karger.com/Services/RightsPermissions
dcterms.rightsHolderKarger
unesp.author.lattes5016839015394547
unesp.author.lattes1590971576309420
unesp.author.lattes4463138671998432
unesp.campusUniversidade Estadual Paulista (Unesp), Instituto de Biociências, Botucatupt
unesp.campusUniversidade Estadual Paulista (Unesp), Faculdade de Medicina, Botucatupt

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Artigos - Clínica Médica - FMB
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