Glycobiology Advance Access originally published online on August 22, 2008
Glycobiology 2008 18(11):842-850; doi:10.1093/glycob/cwn079
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Degeneration of dystrophic or injured skeletal muscles induces high expression of Galectin-1
3 Muscular Dystrophy Research Center (AADM/UNAERP), School of Medicine, University of Ribeirão Preto, 14096-900 Ribeirão Preto-SP, Brazil
4 Departamento de Análises Clínicas, Toxicológicas e Bromatológicas da Faculdade de Ciências Farmacêuticas de Ribeirão Preto, University of Sao Paulo, 14040-903 Ribeirão Preto-SP, Brazil
5 Department of Biochemistry and Molecular Biology, Oklahoma Center for Medical Glycobiology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA
6 Department of Biochemistry, Emory University School of Medicine Atlanta, Atlanta, GA 30322, USA
7 Department of Cellular and Molecular Biology, School of Medicine of Ribeirão Preto, University of São Paulo, 14049-900 Ribeirão Preto-SP, Brazil
1 To whom correspondence should be addressed: Tel/Fax: +55-16-3919-3028; e-mail: mcrcosta{at}usp.br
Received on November 28, 2007; revised on August 11, 2008; accepted on August 13, 2008
Muscle degenerative diseases such as Duchenne Muscular Dystrophy are incurable and treatment options are still restrained. Understanding the mechanisms and factors responsible for muscle degeneration and regeneration will facilitate the development of novel therapeutics. Several recent studies have demonstrated that Galectin-1 (Gal-1), a carbohydrate-binding protein, induces myoblast differentiation and fusion in vitro, suggesting a potential role for this mammalian lectin in muscle regenerative processes in vivo. However, the expression and localization of Gal-1 in vivo during muscle injury and repair are unclear. We report the expression and localization of Gal-1 during degenerative–regenerative processes in vivo using two models of muscular dystrophy and muscle injury. Gal-1 expression increased significantly during muscle degeneration in the murine mdx and in the canine Golden Retriever Muscular Dystrophy animal models. Compulsory exercise of mdx mouse, which intensifies degeneration, also resulted in sustained Gal-1 levels. Furthermore, muscle injury of wild-type C57BL/6 mice, induced by BaCl2 treatment, also resulted in a marked increase in Gal-1 levels. Increased Gal-1 levels appeared to localize both inside and outside the muscle fibers with significant extracellular Gal-1 colocalized with infiltrating CD45+ leukocytes. By contrast, regenerating muscle tissue showed a marked decrease in Gal-1 to baseline levels. These results demonstrate significant regulation of Gal-1 expression in vivo and suggest a potential role for Gal-1 in muscle homeostasis and repair.
Key words: Duchenne Muscular Dystrophy / degeneration–regeneration / galectin-1 / skeletal muscle / mdx mice
2 These authors contributed equally to this work
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