Cerri, Daniel G.
Rodrigues, Lilian C.
Stowell, Sean R.
Araujo, Daniela D.
Coelho, Mariana C.
Oliveira, Sibere R.
Bizario, Joao C. S.
Cummings, Richard D.
Costa, Maria Cristina R.
Total Authors: 10
 Univ Ribeirao Preto, Sch Med, UNAERP, Muscular Dystrophy Res Ctr, AADM, BR-14096900 Ribeirao Preto, SP - Brazil
 Univ Sao Paulo, Fac Ciencias Farmaceut, Dep Anal Clin Toxicol & Bromatol, BR-14040903 Ribeirao Preto, SP - Brazil
 Emory Univ, Sch Med, Dept Biochem, Atlanta, GA 30322 - USA
 Univ Oklahoma, Hlth Sci Ctr, Oklahoma Ctr Med Glycobiol, Dept Biochem & Mol Biol, Oklahoma City, OK 73104 - USA
 Univ Sao Paulo, Sch Med, Dept Cellular & Mol Biol, BR-14049900 Ribeirao Preto, SP - Brazil
Total Affiliations: 5
Web of Science Citations:
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 BaCl(2) 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. (AU)