Evidence of mdx mouse skeletal muscle fragility in vivo by eccentric running exercise.
Muscle Nerve
; 21(5): 567-76, 1998 May.
Article
en En
| MEDLINE
| ID: mdl-9572235
ABSTRACT
Duchenne muscular dystrophy is an X-linked devastating disease due to the lack of expression of a functional dystrophin. Unfortunately, the dystrophin-deficient mdx mouse model does not present clinical signs of dystrophy before the age of 18 months, and the role of dystrophin in fiber integrity is not fully understood. The fragility of the skeletal muscle fibers was investigated in transgenic mice expressing beta-galactosidase under the control of a muscle specific promoter. Adult mdx/beta-galactosidase (dystrophin-negative) and normal/beta-galactosidase (dystrophin-positive) mice were submitted to one short session of eccentric, downhill running exercise. The leakage of muscle enzymes creatine kinase and beta-galactosidase was investigated before, 1 h after, and 3 days after the running session. A significant and transient rise in the level of these enzymes was noted in the serum of mdx mice following the exercise session. Thus, the lack of dystrophin in the mdx model led to local microdamages to the exercised muscle allowing leakage of proteins from the fibers. The peak leakage was transient, suggesting that muscle fiber lesions were rapidly repaired following this short, noninvasive eccentric running session.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Carrera
/
Ratones Endogámicos mdx
/
Músculo Esquelético
Límite:
Animals
Idioma:
En
Revista:
Muscle Nerve
Año:
1998
Tipo del documento:
Article
País de afiliación:
Canadá