scholarly journals Evaluation of Muscle Function of the Extensor Digitorum Longus Muscle Ex vivo and Tibialis Anterior Muscle In situ in Mice

10.3791/50183 ◽  
2013 ◽  
Author(s):  
Chady H. Hakim ◽  
Nalinda B. Wasala ◽  
Dongsheng Duan
Keyword(s):  
Muscle Function ◽  
Tibialis Anterior ◽  
Extensor Digitorum Longus ◽  
Ex Vivo ◽  
Tibialis Anterior Muscle ◽  
Extensor Digitorum Longus Muscle ◽  
Extensor Digitorum ◽  
Longus Muscle

Progressive deterioration of muscles in mdx mice induced by overload

1993 ◽  
Vol 84 (2) ◽  
pp. 145-150 ◽  
Author(s):  
J. Dick ◽  
G. Vrbová
Keyword(s):  
Tibialis Anterior ◽  
Extensor Digitorum Longus ◽  
Tibialis Anterior Muscle ◽  
Young Group ◽  
Extensor Digitorum Longus Muscle ◽  
Extensor Digitorum ◽  
Mdx Mice ◽  
Normal Strain ◽  
Longus Muscle ◽  
Twitch And Tetanic Tensions

1. Extensor digitorum longus muscles of C57 BL/10 and mdx mice were overloaded by removing the synergist tibialis anterior muscle of 9–12-day-old animals. The effect of this operation on the weight, contractile properties and force of the extensor digitorum longus muscle was examined at two different ages, i.e. at 2–3 months (young group) and at 5–8 months (old group). The changes with age in both the control and overloaded muscles of normal and mdx mice are also described. The values obtained from the overloaded muscles were always compared with those for the control, unoperated extensor digitorum longus. 2. In the normal strain of mice the weight of the overloaded extensor digitorum longus muscle in the younger group was increased and it remained higher in the older animals. In the mdx mice the overloaded extensor digitorum longus muscles weighed more in the younger animals but not in the older group of mice. 3. The twitch and tetanic tensions of the overloaded muscles were slightly, but not significantly, increased in the younger group of mdx mice, whereas in the older animals there was a significant decrease in both twitch and tetanic tensions. 4. Thus the overloaded muscles from mdx mice progressively deteriorated with age. In both strains of mice the overloaded muscles become less fatiguable with time.

Catalase overexpression does not impair extensor digitorum longus muscle function in normal mice

2007 ◽  
Vol 36 (6) ◽  
pp. 833-841 ◽  
Author(s):  
Mingju Liu ◽  
Yongping Yue ◽  
Dejia Li ◽  
Dongsheng Duan
Keyword(s):  
Muscle Function ◽  
Extensor Digitorum Longus ◽  
Extensor Digitorum Longus Muscle ◽  
Extensor Digitorum ◽  
Longus Muscle

scholarly journals Alpha 7 integrin preserves the function of the extensor digitorum longus muscle in dystrophin-null mice

2013 ◽  
Vol 115 (9) ◽  
pp. 1388-1392 ◽  
Author(s):  
Chady H. Hakim ◽  
Dean J. Burkin ◽  
Dongsheng Duan
Keyword(s):  
Muscular Dystrophy ◽  
Knockout Mice ◽  
Muscle Function ◽  
Extensor Digitorum Longus ◽  
Transmission Loss ◽  
Extensor Digitorum Longus Muscle ◽  
Extensor Digitorum ◽  
Force Transmission ◽  
Double Knockout ◽  
Longus Muscle

The dystrophin-associated glycoprotein complex (DGC) and the α7β1-integrin complex are two independent protein complexes that link the extracellular matrix with the cytoskeleton in muscle cells. These associations stabilize the sarcolemma during force transmission. Loss of either one of these complexes leads to muscular dystrophy. Dystrophin is a major component of the DGC. Its absence results in Duchenne muscular dystrophy (DMD). Because α7-integrin overexpression has been shown to ameliorate muscle histopathology in mouse models of DMD, we hypothesize that the α7β1-integrin complex can help preserve muscle function. To test this hypothesis, we evaluated muscle force, elasticity, and the viscous property of the extensor digitorum longus muscle in 19-day-old normal BL6, dystrophin-null mdx4cv, α7-integrin-null, and dystrophin/α7-integrin double knockout mice. While nominal changes were found in single knockout mice, contractility and passive properties were significantly compromised in α7-integrin double knockout mice. Our results suggest that DGC and α7β1-integrin complexes may compensate each other to maintain normal skeletal muscle function. α7β1-Integrin upregulation may hold promise to treat not only histological, but also physiological, defects in DMD.

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