Degeneration of dystrophic or injured skeletal muscles induces high expression of Galectin-1.

Glycobiology
Daniel G CerriMaria Cristina R Costa

Abstract

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 outsid...Continue Reading

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Citations

Dec 24, 2008·The Journal of Biological Chemistry·Sean R StowellRichard D Cummings
Jun 11, 2009·Journal of Neuroimmunology·João Carlos da Silva BizarioMaria Cristina Ramos Costa
Jun 9, 2015·Molecular Therapy : the Journal of the American Society of Gene Therapy·Pam M Van RyDean J Burkin
Sep 2, 2016·Proteomics·Nourine A KamiliSean R Stowell
Apr 21, 2017·The Journal of Biological Chemistry·Nam D PhamJennifer J Kohler
Aug 24, 2019·Frontiers in Immunology·Brian S RobinsonSean R Stowell
Aug 16, 2017·Journal of Proteome Research·Caroline BarbéJean-Paul Thissen
Jul 6, 2021·Glycobiology·Daniel Giuliano CerriMarcelo Dias-Baruffi

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