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Please use this identifier to cite or link to this item: http://acervodigital.unesp.br/handle/11449/117256
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dc.contributor.authorRuiz Lima, Aline Regina-
dc.contributor.authorMartinez, Paula Felippe-
dc.contributor.authorDamatto, Ricardo Luiz-
dc.contributor.authorMariano Cezar, Marcelo Diarcadia-
dc.contributor.authorGuizoni, Daniele Mendes-
dc.contributor.authorBonomo, Camila-
dc.contributor.authorOliveira, Silvio Assis-
dc.contributor.authorSilva, Maeli Dal-Pai-
dc.contributor.authorZornoff, Leonardo Antonio Mamede-
dc.contributor.authorOkoshi, Katashi-
dc.contributor.authorOkoshi, Marina Politi-
dc.date.accessioned2015-03-18T15:55:39Z-
dc.date.accessioned2016-10-25T20:34:54Z-
dc.date.available2015-03-18T15:55:39Z-
dc.date.available2016-10-25T20:34:54Z-
dc.date.issued2014-01-01-
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.issn1015-8987-
dc.identifier.urihttp://hdl.handle.net/11449/117256-
dc.identifier.urihttp://acervodigital.unesp.br/handle/11449/117256-
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.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)-
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)-
dc.format.extent333-345-
dc.language.isoeng-
dc.publisherKarger-
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.typeoutro-
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)-
dc.contributor.institutionUniversidade Federal de Mato Grosso do Sul (UFMS)-
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.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.identifier.doi10.1159/000363003-
dc.identifier.wosWOS:000343764600010-
dc.rights.accessRightsAcesso aberto-
dc.identifier.fileWOS000343764600010.pdf-
dc.relation.ispartofCellular Physiology And Biochemistry-
Appears in Collections:Artigos, TCCs, Teses e Dissertações da Unesp

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