ArticleThe American journal of pathology2015
Deletion of Galgt2 (B4Galnt2) reduces muscle growth in response to acute injury and increases muscle inflammation and pathology in dystrophin-deficient mice.
Article in The American journal of pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 26 citations in OpenAlex.
- Exercise Training Reduces the Inflammatory Response and Promotes Intestinal Mucosa-Associated Immunity in Lynch Syndrome.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023Trial
- Emerging Roles of Dystroglycan in Cardiac Remodeling, Fibrosis, and Heart Failure.International journal of molecular sciences · 2026Review
- Dystrophin Restorative and Compensatory Gene Addition Therapies for Duchenne Muscular Dystrophy: Could CRISPRa Provide a Realistic Alternative?Muscles (Basel, Switzerland) · 2025Review
- Review
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- A first-in-human phase I/IIa gene transfer clinical trial for Duchenne muscular dystrophy using rAAVrh74.MCK.Molecular therapy. Methods & clinical development · 2022Article
- The role of protein glycosylation in muscle diseases.Molecular biology reports · 2022Review
- Sarcospan increases laminin-binding capacity of α-dystroglycan to ameliorate DMD independent of Galgt2.Human molecular genetics · 2022Article
- The Cancer-Associated Antigens Sialyl LewisCancers · 2021Review
- Serum Antibodies to N-Glycolylneuraminic Acid Are Elevated in Duchenne Muscular Dystrophy and Correlate with Increased Disease Pathology in CmahThe American journal of pathology · 2021Article
- Current Pharmacological Strategies for Duchenne Muscular Dystrophy.Frontiers in cell and developmental biology · 2021Review
- Article
- Genetic modifiers and phenotypic variability in neuromuscular disorders.Journal of applied genetics · 2020Review
- rAAVrh74.MCK.Molecular therapy. Methods & clinical development · 2019Article
- Soluble Heparin Binding Epidermal Growth Factor-Like Growth Factor Is a Regulator ofMolecular and cellular biology · 2019Article
- rAAVrh74.MCK.GALGT2 Protects against Loss of Hemodynamic Function in the Aging mdx Mouse Heart.Molecular therapy : the journal of the American Society of Gene Therapy · 2019Article
- An Isolated Limb Infusion Method Allows for Broad Distribution of rAAVrh74.MCK.Molecular therapy. Methods & clinical development · 2018Article
- Comparative Transcriptomics Identifies Novel Genes and Pathways Involved in Post-Traumatic Osteoarthritis Development and Progression.International journal of molecular sciences · 2018Article
- Embryoglycan: a highly branched poly-N-acetyllactosamine in pluripotent stem cells and early embryonic cells.Glycoconjugate journal · 2017Review
- Induction of T-Cell Infiltration and Programmed Death Ligand 2 Expression by Adeno-Associated Virus in Rhesus Macaque Skeletal Muscle and Modulation by Prednisone.Human gene therapy · 2017Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Transgenic overexpression of Galgt2 (official name B4Galnt2) in skeletal muscle stimulates the glycosylation of α dystroglycan (αDG) and the up-regulation of laminin α2 and dystrophin surrogates known to inhibit muscle pathology in mouse models of congenital muscular dystrophy 1A and Duchenne muscular dystrophy. Skeletal muscle Galgt2 gene expression is also normally increased in the mdx mouse model of Duchenne muscular dystrophy compared with the wild-type mice. To assess whether this increased endogenous Galgt2 expression could affect disease, we quantified muscular dystrophy measures in mdx mice deleted for Galgt2 (Galgt2(-/-)mdx). Galgt2(-/-) mdx mice had increased heart and skeletal muscle pathology and inflammation, and also worsened cardiac function, relative to age-matched mdx mice. Deletion of Galgt2 in wild-type mice also slowed skeletal muscle growth in response to acute muscle injury. In each instance where Galgt2 expression was elevated (developing muscle, regenerating muscle, and dystrophic muscle), Galgt2-dependent glycosylation of αDG was also increased. Overexpression of Galgt2 failed to inhibit skeletal muscle pathology in dystroglycan-deficient muscles, in contrast to previous studies in dystrophin-deficient mdx muscles. This study demonstrates that Galgt2 gene expression and glycosylation of αDG are dynamically regulated in muscle and that endogenous Galgt2 gene expression can ameliorate the extent of muscle pathology, inflammation, and dysfunction in mdx mice.
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