ArticleThe American journal of pathology2009
Laminin-111 restores regenerative capacity in a mouse model for alpha7 integrin congenital myopathy.
Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 69 citations in OpenAlex.
- Article
- Duchenne muscular dystrophy: disease mechanism and therapeutic strategies.Frontiers in physiology · 2023Review
- Skeletal Muscle Regeneration in Cardiotoxin-Induced Muscle Injury Models.International journal of molecular sciences · 2022Review
- Association between Decreased ITGA7 Levels and Increased Muscle α-Synuclein in an MPTP-Induced Mouse Model of Parkinson's Disease.International journal of molecular sciences · 2022Article
- Muscle stem cell polarity requires QKI-mediated alternative splicing of Integrin Alpha-7 (Itga7).Life science alliance · 2022Article
- Biomimetic sponges improve muscle structure and function following volumetric muscle loss.Journal of biomedical materials research. Part A · 2021Article
- Laminin-111 protein therapy after disease onset slows muscle disease in a mouse model of laminin-α2 related congenital muscular dystrophy.Human molecular genetics · 2020Article
- Implications of Skeletal Muscle Extracellular Matrix Remodeling in Metabolic Disorders: Diabetes Perspective.International journal of molecular sciences · 2020Review
- Cross-Talk Between Extracellular Matrix and Skeletal Muscle: Implications for Myopathies.Frontiers in pharmacology · 2020Review
- Zebrafish Models ofFrontiers in molecular neuroscience · 2020Article
- Laminin and Integrin in LAMA2-Related Congenital Muscular Dystrophy: From Disease to Therapeutics.Frontiers in molecular neuroscience · 2020Article
- Review
- Laminin-111 protein therapy enhances muscle regeneration and repair in the GRMD dog model of Duchenne muscular dystrophy.Human molecular genetics · 2019Article
- Cellular rescue in a zebrafish model of congenital muscular dystrophy type 1A.NPJ Regenerative medicine · 2019Article
- Current understanding and treatment of cardiac and skeletal muscle pathology in laminin-α2 chain-deficient congenital muscular dystrophy.The application of clinical genetics · 2019Article
- Chimeric protein identification of dystrophic, Pierson and other laminin polymerization residues.Matrix biology : journal of the International Society for Matrix Biology · 2018Article
- Basal lamina remodeling at the skeletal muscle stem cell niche mediates stem cell self-renewal.Nature communications · 2018Article
- Engineered matrices for skeletal muscle satellite cell engraftment and function.Matrix biology : journal of the International Society for Matrix Biology · 2017Review
- Impaired fetal muscle development and JAK-STAT activation mark disease onset and progression in a mouse model for merosin-deficient congenital muscular dystrophy.Human molecular genetics · 2017Article
- Increased Expression of Laminin Subunit Alpha 1 Chain by dCas9-VP160.Molecular therapy. Nucleic acids · 2017Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Mutations in the alpha7 integrin gene cause congenital myopathy characterized by delayed developmental milestones and impaired mobility. Previous studies in dystrophic mice suggest the alpha7beta1 integrin may be critical for muscle repair. To investigate the role that alpha7beta1 integrin plays in muscle regeneration, cardiotoxin was used to induce damage in the tibialis anterior muscle of alpha7 integrin-null mice. Unlike wild-type muscle, which responded rapidly to repair damaged myofibers, alpha7 integrin-deficient muscle exhibited defective regeneration. Analysis of Pax7 and MyoD expression revealed a profound delay in satellite cell activation after cardiotoxin treatment in alpha7 integrin-null animals when compared with wild type. We have recently demonstrated that the muscle of alpha7 integrin-null mice exhibits reduced laminin-alpha2 expression. To test the hypothesis that loss of laminin contributes to the defective muscle regeneration phenotype observed in alpha7 integrin-null mice, mouse laminin-111 (alpha1, beta1, gamma1) protein was injected into the tibialis anterior muscle 3 days before cardiotoxin-induced injury. The injected laminin-111 protein infiltrated the entire muscle and restored myogenic repair and muscle regeneration in alpha7 integrin-null muscle to wild-type levels. Our data demonstrate a critical role for a laminin-rich microenvironment in muscle repair and suggest laminin- 111 protein may serve as an unexpected and novel therapeutic agent for patients with congenital myopathies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.