ArticleThe American journal of pathology2011
Transgenic expression of Laminin α1 chain does not prevent muscle disease in the mdx mouse model for Duchenne muscular dystrophy.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- Duchenne muscular dystrophy: disease mechanism and therapeutic strategies.Frontiers in physiology · 2023Review
- From Mice to Humans: An Overview of the Potentials and Limitations of Current Transgenic Mouse Models of Major Muscular Dystrophies and Congenital Myopathies.International journal of molecular sciences · 2020Review
- Laminin and Integrin in LAMA2-Related Congenital Muscular Dystrophy: From Disease to Therapeutics.Frontiers in molecular neuroscience · 2020Article
- Laminin-deficient muscular dystrophy: Molecular pathogenesis and structural repair strategies.Matrix biology : journal of the International Society for Matrix Biology · 2018Review
- Increased Expression of Laminin Subunit Alpha 1 Chain by dCas9-VP160.Molecular therapy. Nucleic acids · 2017Article
- Laminin 521 maintains differentiation potential of mouse and human satellite cell-derived myoblasts during long-term culture expansion.Skeletal muscle · 2016Article
- Genome-wide association study to identify potential genetic modifiers in a canine model for Duchenne muscular dystrophy.BMC genomics · 2016Article
- Laminin-111 improves skeletal muscle stem cell quantity and function following eccentric exercise.Stem cells translational medicine · 2014Article
- Glia unglued: how signals from the extracellular matrix regulate the development of myelinating glia.Developmental neurobiology · 2011Review
- Forced expression of laminin beta1 in podocytes prevents nephrotic syndrome in mice lacking laminin beta2, a model for Pierson syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- The dystrophin-glycoprotein complex in the prevention of muscle damage.Journal of biomedicine & biotechnology · 2011Review
- Laminin-211 in skeletal muscle function.Cell adhesion & migrationReview
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Duchenne muscular dystrophy (DMD) is a severe neuromuscular disorder, and one of the most frequently encountered, but one for which there is as yet no treatment. Laminin-111 protein therapy was recently shown to be a promising approach to prevent muscle disease in the mdx mouse model of DMD. The present study demonstrated that transgenic expression of laminin α1 chain in mdx animals, resulting in laminin-111 heterotrimer formation in mdx muscle, does not improve the dystrophic phenotype. The mdx mice overexpressing laminin-111 (mdxLMα1) display features of mdx littermates: dystrophic pattern of muscle biopsy, elevated creatine kinase levels, reduced muscle strength, and decreased sarcolemmal integrity. Increased expression of integrin α7 is not beneficial for mdxLMα1 muscle, and components of the dystrophin-glycoprotein complex are not restored at the sarcolemma on laminin-111 overexpression. In summary, further studies are needed to verify the functionality of laminin-111 protein therapy in DMD and to describe the molecular events resulting from this approach.
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