Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/237990
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dc.contributor.CRUESPUNIVERSIDADE DE ESTADUAL DE CAMPINASpt_BR
dc.typeArtigo de periódicopt_BR
dc.titleDiaphragm Degeneration And Cardiac Structure In Mdx Mouse: Potential Clinical Implications For Duchenne Muscular Dystrophypt_BR
unicamp.authorBarbin, I.C.C., Departamento de Biologia Estrutural e Funcional Instituto de Biologia Universidade Estadual de Campinas (UNICAMP) Campinas, São Paulo Brazilpt_BR
unicamp.authorPereira, J.A., Departamento de Biologia Estrutural e Funcional Instituto de Biologia Universidade Estadual de Campinas (UNICAMP) Campinas, São Paulo Brazilpt_BR
unicamp.authorBersan Rovere, M., Departamento de Biologia Estrutural e Funcional Instituto de Biologia Universidade Estadual de Campinas (UNICAMP) Campinas, São Paulo Brazilpt_BR
unicamp.authorde Oliveira Moreira, D., Departamento de Biologia Estrutural e Funcional Instituto de Biologia Universidade Estadual de Campinas (UNICAMP) Campinas, São Paulo Brazilpt_BR
unicamp.authorMarques, M.J., Departamento de Biologia Estrutural e Funcional Instituto de Biologia Universidade Estadual de Campinas (UNICAMP) Campinas, São Paulo Brazilpt_BR
unicamp.authorSanto Neto, H., Departamento de Biologia Estrutural e Funcional Instituto de Biologia Universidade Estadual de Campinas (UNICAMP) Campinas, São Paulo Brazilpt_BR
dc.description.abstractWe examined the effects of exercise on diaphragm degeneration and cardiomyopathy in dystrophin-deficient mdx mice. Mdx mice (11 months of age) were exercised (swimming) for 2 months to worsen diaphragm degeneration. Control mdx mice were kept sedentary. Morphological evaluation demonstrated increased fibrosis in the diaphragm of exercised mdx mice (33.3 ± 6.0% area of fibrosis) compared with control mdx mice (20.9 ± 1.7% area of fibrosis). Increased (26%) activity of MMP-2, a marker of fibrosis, was detected in the diaphragms from exercised mdx mice. Morphological evaluation of the heart demonstrated a 45% increase in fibrosis in the right ventricle (8.3 ± 0.6% in sedentary vs. 12.0 ± 0.6% of fibrosis in exercised) and in the left ventricle (35% increase) in the exercised mdx mice. The density of inflammatory cells-degenerating cardiomyocytes increased 95% in the right ventricle (2.3 ± 0.6 in sedentary vs. 4.5 ± 0.8 in exercised) and 71% in the left ventricle (1.4 ± 0.6 sedentary vs. 2.4 ± 0.5 exercised). The levels of both active MMP-2 and the pro-fibrotic factor transforming growth factor beta were elevated in the hearts of exercised compared with sedentary mdx mice. The wall thickness to lumen diameter ratio of the pulmonary trunk was significantly increased in the exercised mdx mice (0.11 ± 0.04 in sedentary vs. 0.28 ± 0.12 in exercised), as was the thickness of the right ventricle wall, which suggests the occurrence of pulmonary hypertension in those animals. It is suggested that diaphragm degeneration is a main contributor to right ventricle dystrophic pathology. These findings may be relevant for future interventional studies for Duchenne muscular dystrophy-associated cardiomyopathy. © 2016 Anatomical Society.en
dc.relation.ispartofJournal of Anatomypt_BR
dc.publisherBlackwell Publishing Ltdpt_BR
dc.date.issued2016pt_BR
dc.identifier.citationJournal Of Anatomy. Blackwell Publishing Ltd, v. 228, n. 5, p. 784 - 791, 2016.pt_BR
dc.language.isoenpt_BR
dc.description.volume228pt_BR
dc.description.issuenumber5pt_BR
dc.description.firstpage784pt_BR
dc.description.lastpage791pt_BR
dc.rightsfechadopt_BR
dc.sourceScopuspt_BR
dc.identifier.issn218782pt_BR
dc.identifier.doi10.1111/joa.12443pt_BR
dc.identifier.urlhttp://www.scopus.com/inward/record.url?eid=2-s2.0-84956705206&partnerID=40&md5=b4ab3cd5aeb9c2145efdf4487ece234fpt_BR
dc.date.available2016-06-03T20:13:10Z-
dc.date.accessioned2016-06-03T20:13:10Z-
dc.description.provenanceMade available in DSpace on 2016-06-03T20:13:10Z (GMT). No. of bitstreams: 1 2-s2.0-84956705206.pdf: 962650 bytes, checksum: 97065a1d8061050e6ea275c53966398e (MD5) Previous issue date: 2016en
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/237990-
dc.identifier.idScopus2-s2.0-84956705206pt_BR
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