Severe muscle dysfunction precedes collagen tissue proliferation in mdx mouse diaphragm

Author:

Coirault Catherine1,Pignol Bernadette2,Cooper Racquel N.3,Butler-Browne Gillian3,Chabrier Pierre-Etienne2,Lecarpentier Yves14

Affiliation:

1. Institut National de la Santé et de la Recherche Médicale, Laboratoire d'Optique Appliquée, Ecole Nationale Supérieure de Techniques Avancées, Ecole Polytechnique, 91761 Palaiseau;

2. Institut Henri Beaufour, 91966 Les Ulis;

3. UnitéMixte de Recherche, Centre National de la Recherche Scientifique 7000, 75634 Paris; and

4. Service d'Explorations Cardio-Respiratoires, Hôpital de Bicêtre, Assistance Publique-Hôpitaux de Paris, 94275 Le Kremlin-Bicêtre, France

Abstract

After extensive necrosis, progressive diaphragm muscle weakness in the mdx mouse is thought to reflect progressive replacement of contractile tissue by fibrosis. However, little has been documented on diaphragm muscle performance at the stage at which necrosis and fibrosis are limited. Diaphragm morphometric characteristics, muscle performance, and cross-bridge (CB) properties were investigated in 6-wk-old control (C) and mdx mice. Compared with C, maximum tetanic tension and shortening velocity were 37 and 32% lower, respectively, in mdx mice (each P < 0.05). The total number of active CB per millimeter squared (13.0 ± 1.2 vs. 18.4 ± 1.7 × 109/mm2, P < 0.05) and the CB elementary force (8.0 ± 0.2 vs. 9.0 ± 0.1 pN, P < 0.01) were lower in mdx than in C. The time cycle duration was lower in mdx than in C (127 ± 18 vs. 267 ± 61 ms, P < 0.05). Percentages of fiber necrosis represented 2.8 ± 0.6% of the total muscle fibers, and collagen surface area occupied 3.6 ± 0.7% in mdx diaphragm. Our results pointed to severe muscular dysfunction in mdx mouse diaphragm, despite limited necrotic and fibrotic lesions.

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology

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