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http://dx.doi.org/10.5352/JLS.2016.26.5.592

Dystrophin Degradation in Skeletal Muscles with Lipid Enrichment in Cattle  

Jeon, Sung-Hwan (Department of Veterinary Pathology, College of Veterinary Medicine, Kyungpook National University)
Kim, Ah-Young (Department of Veterinary Pathology, College of Veterinary Medicine, Kyungpook National University)
Lee, Eun-Mi (Department of Veterinary Pathology, College of Veterinary Medicine, Kyungpook National University)
Lee, Eun-Joo (Department of Veterinary Pathology, College of Veterinary Medicine, Kyungpook National University)
Hong, Il-Hwa (Department of Veterinary Pathology, College of Veterinary Medicine, Kyungpook National University)
Hwang, Ok-Kyung (Department of Veterinary Pathology, College of Veterinary Medicine, Kyungpook National University)
Jeong, Kyu-Shik (Department of Veterinary Pathology, College of Veterinary Medicine, Kyungpook National University)
Publication Information
Journal of Life Science / v.26, no.5, 2016 , pp. 592-602 More about this Journal
Abstract
This study investigated the muscular dystrophin levels in freely moving Australian cattle mainly fed grass, freely moving Korean cattle fed mainly a grain diet, and Korean cattle fed a grain diet but housed in a relatively limited space of a cow house. The total skeletal muscle specimens of 244 cattle were collected and immediately fixed in 10% neutral formalin. The same area was biopsied from the cattle in both countries. The findings showed that fatty infiltration is highly correlated with membrane-associated protein degradation in skeletal muscle, and that among several membrane-associated proteins, dystrophin showed the most significant reduction in expression in the cattle with fatty infiltration. Similarly, CD36 was more highly expressed in the cattle with fatty infiltration of skeletal muscle. Various breeding factors, such as oxidative stress; the presence of oxidized lipids in the diet; and environmental factors such as exercise, temperature and amount of time spent, may have critical effects on the degradation of normal cytoskeleton proteins, which are required for maintaining normal skeletal muscle architecture. Among the sarcolemma membrane-associated proteins, dystrophin is the most sensitive membrane protein that is involved muscular dystrophy and muscular degeneration. Thus, the present findings may be useful for studies on muscular dystrophy in humans or the pathogenesis of muscular diseases in animal models.
Keywords
Cattle; dystrophin; dystrophy; lipid; muscle;
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1 Abutarbush, S. M. and Radostits, O. M. 2003. Congenital nutritional muscular dystrophy in a beef calf. Can. Vet. J. 44, 738-739.
2 Al-Ruwaishid, A., Vajsar, J., Tein, I., Benson, L. and Jay, V. 2003. Centronuclear myopathy and cardiomyopathy requiring heart transplant. Brain Dev. 25, 62-66.   DOI
3 Bansal, D. and Campbell, K. P. 2004. Dysferlin and the plasma membrane repair in muscular dystrophy. Trends Cell Biol. 14, 206-213.   DOI
4 Barton, E. R. 2006. Impact of sarcoglycan complex on mechanical signal transduction in murine skeletal muscle. Am. J. Physiol. Cell. Physiol. 290, C411-9.
5 Blake, D. J., Weir, A., Newey, S. E. and Davies, K. E. 2002. Function and genetics of dystrophin and dystrophin-related proteins in muscle. Physiol. Rev. 82, 291-329.   DOI
6 Bonnal, C., Raynaud, F., Astier, C., Lebart, M. C., Marcilhac, A., Coves, D., Corraze, G., Gelineau, A., Fleurence, J., Roustan, C. and Benyamin, Y. 2001. Postmortem degradation of white fish skeletal muscle (sea bass, Dicentrarchus labrax): fat diet effects on in situ dystrophin proteolysis during the prerigor stage. Mar. Biotechnol. (NY). 3, 172-180.   DOI
7 Drover, V. A. and Abumrad, N. A. 2005. CD36-dependent fatty acid uptake regulates expression of peroxisome proliferator activated receptors. Biochem. Soc. Trans. 33, 311-315.   DOI
8 Eichhorn, J. M., Coleman, L. J., Wakayama, E. J., Blomquist, G. J., Bailey, C. M. and Jenkins, T. G. 1986. Effects of breed type and restricted versus ad libitum feeding on fatty acid composition and cholesterol content of muscle and adipose tissue from mature bovine females. J. Anim. Sci. 63, 781-794.   DOI
9 Ervasti, J. M. and Campbell, K. P. 1993. Dystrophin and the membrane skeleton. Curr. Opin. Cell Biol. 5, 82-87.   DOI
10 Fairclough, R. J., Wood, M. J. and Davies, K. E. 2013. Therapy for Duchenne muscular dystrophy: renewed optimism from genetic approaches. Nat. Rev. Genet. 14, 373-378.   DOI
11 Ferrari, R., Merli, E., Cicchitelli, G., Mele, D., Fucili, A. and Ceconi, C. 2004. Therapeutic effects of L-carnitine and propionyl-L-carnitine on cardiovascular diseases: a review. Ann. N. Y. Acad. Sci. 1033, 79-91.   DOI
12 Freund, A. A., Scola, R. H., Arndt, R. C., Lorenzoni, P. J., Kay, C. K. and Werneck, L. C. 2007. Duchenne and Becker muscular dystrophy: a molecular and immunohistochemical approach. Arq. Neuropsiquiatr. 65, 73-76.   DOI
13 Keizer, H. A., Schaart, G., Tandon, N. N., Glatz, J. F. and Luiken, J. J. 2004. Subcellular immunolocalisation of fatty acid translocase (FAT)/CD36 in human type-1 and type-2 skeletal muscle fibres. Histochem. Cell Biol. 121, 101-107.   DOI
14 Kovac, G., Mudron, P., Prosbova, M. and Pasteka, J. 1987. Clinical and biochemical response in the prevention of nutritional myodystrophy in heifers. Vet. Med. (Praha). 32, 81-92.
15 Kuehn, B. M. 2007. Studies point way to new therapeutic prospects for muscular dystrophy. JAMA 298, 1385-1386.
16 Kumar, A., Khandelwal, N., Malya, R., Reid, M. B. and Boriek, A. M. 2004. Loss of dystrophin causes aberrant mechanotransduction in skeletal muscle fibers. FASEB J. 18, 102- 113.   DOI
17 Muntoni, F. and Wells, D. 2007. Genetic treatments in muscular dystrophies. Curr. Opin. Neurol. 20, 590-594.   DOI
18 Langohr, I. M., Stevenson, G. W. and Valentine, B. A. 2007. Muscular pseudohypertrophy (steatosis) in a bovine fetus. J. Vet. Diagn. Invest. 19, 198-201.   DOI
19 Messina, S., Altavilla, D., Aguennouz, M., Seminara, P., Minutoli, L., Monici, M. C., Bitto, A., Mazzeo, A., Marini, H., Squadrito, F. and Vita, G. 2006. Lipid peroxidation inhibition blunts nuclear factor-kappaB activation, reduces skeletal muscle degeneration, and enhances muscle function in mdx mice. Am. J. Pathol. 168, 918-926.   DOI
20 Mokhtarian, A., Lefaucheur, J. P., Even, P. C. and Sebille, A. 1995. Effects of treadmill exercise and high-fat feeding on muscle degeneration in mdx mice at the time of weaning. Clin. Sci. (Lond). 89, 447-452.   DOI
21 Nockels, C. F., Odde, K. G. and Craig, A. M. 1996. Vitamin E supplementation and stress affect tissue alpha-tocopherol content of beef heifers. J. Anim. Sci. 74, 672-677.   DOI
22 Park, J. K., Ki, M. R., Lee, H. R., Hong, I. H., Ji, A. R., Ishigami, A., Park, S. I., Kim, J. M., Chung, H. Y., Yoo, S. E. and Jeong, K. S. 2010. Vitamin C deficiency attenuates liver fibrosis by way of up-regulated peroxisome proliferator-activated receptor-gamma expression in senescence marker protein 30 knockout mice. Hepatology 51, 1766-1777.   DOI
23 Rodino-Klapac, L. R., Chicoine, L. G., Kaspar, B. K. and Mendell, J. R. 2007. Gene therapy for duchenne muscular dystrophy: expectations and challenges. Arch. Neurol. 64, 1236-1241.   DOI
24 Voisin, V. and de la Porte, S. 2004. Therapeutic strategies for Duchenne and Becker dystrophies. Int. Rev. Cytol. 240, 1-30.   DOI
25 Romitti, P. A., Zhu, Y., Puzhankara, S., James, K. A., Nabukera, S. K., Zamba, G. K., Ciafaloni, E., Cunniff, C., Druschel, C. M., Mathews, K. D., Matthews, D. J., Meaney, F. J., Andrews, J. G., Conway, K. M., Fox, D. J., Street, N., Adams, M. M., Bolen, J. and MD STARnet. 2015. Prevalence of Duchenne and Becker muscular dystrophies in the United States. Pediatrics 135, 513-521.   DOI
26 Sampaolesi, M., Blot, S., D′Antona, G., Granger, N., Tonlorenzi, R., Innocenzi, A., Mognol, P., Thibaud, J. L., Galvez, B. G., Barthelemy, I., Perani, L., Mantero, S., Guttinger, M., Pansarasa, O., Rinaldi, C., Cusella De Angelis, M. G., Torrente, Y., Bordignon, C., Bottinelli, R. and Cossu, G. 2006. Mesoangioblast stem cells ameliorate muscle function in dystrophic dogs. Nature 444, 574-579.   DOI
27 Tidball, J. G. and Wehling-Henricks, M. 2007. The role of free radicals in the pathophysiology of muscular dystrophy. J. Appl. Physiol. (1985). 102, 1677-1686.
28 Wein, N., Alfano, L. and Flanigan, K. M. 2015. Genetics and Emerging Treatments for Duchenne and Becker Muscular Dystrophy. Pediatr. Clin. North Am. 62, 723-742.   DOI
29 Wineinger, M. A., Abresch, R. T., Walsh, S. A. and Carter, G. T. 1998. Effects of aging and voluntary exercise on the function of dystrophic muscle from mdx mice. Am. J. Phys. Med. Rehabil. 77, 20-27.   DOI
30 Yamada, M., Takashima, H., Takizawa, T., Mizuno, K., Nakamura, K., Furuoka, H. and Masegi, T. 2004. Congenital myopathy in Japanese Black calves. J. Vet. Med. Sci. 66, 997-1001.   DOI
31 Zust, J., Hrovatin, B. and Simundic, B. 1996. Assessment of selenium and vitamin E deficiencies in dairy herds and clinical disease in calves. Vet. Rec. 139, 391-394.   DOI