Abstract by Hailie Gill
Chemistry and Biochemistry
Pam Van Ry
Effects of Galectin-1 on Myogenesis in Dysferlin-Deficient Cells of LGMD2B
Limb-Girdle Muscular Dystrophy Type 2B (LGMD 2B) is a non-curable, degenerative muscle disease caused by a DYSF gene mutation that results in decreased muscle strength and ineffective membrane repair. This disease affects 1/1,300-1/200,000 people depending on geographic and ethnic origin. Research of a potential protein therapeutic treatment is optimal to decrease LGMD2B disease pathology. Galectin-1 (Gal-1) is a carbohydrate-recognition domain lectin protein involved in cell migration, inflammation, and cell signaling. To determine the effectiveness of Gal-1 in reducing symptoms of LGMD2B, we examined the progression of myogenesis in dysferlin, dysferlin-deficient, and Gal-1 treated dysferlin-deficient cells. Our results indicate that dysferlin-deficient cells treated with Gal-1 show increased levels of late-stage myogenic markers thus stipulating that Gal-1 increases membrane repair and myogenesis. These results may have a potential impact on further treatments of LGMD2B.