Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/236072
Type: Artigo de periódico
Title: Diaphragm Degeneration And Cardiac Structure In Mdx Mouse: Potential Clinical Implications For Duchenne Muscular Dystrophy.
Author: Barbin, Isabel Cristina Chagas
Pereira, Juliano Alves
Bersan Rovere, Matheus
de Oliveira Moreira, Drielen
Marques, Maria Julia
Santo Neto, Humberto
Abstract: We 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.
Subject: Duchenne Muscular Dystrophy
Cardiomyopathy
Fibrosis
Metalloproteinases-2
Citation: Journal Of Anatomy. v. 228, n. 5, 2016-Jan.
Rights: embargo
Identifier DOI: 10.1111/joa.12443
Address: http://www.ncbi.nlm.nih.gov/pubmed/26822140
Date Issue: 2016
Appears in Collections:Unicamp - Artigos e Outros Documentos

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