ArticleAmerican journal of physiology. Cell physiology2008
Increasing alpha 7 beta 1-integrin promotes muscle cell proliferation, adhesion, and resistance to apoptosis without changing gene expression.
Article in American journal of physiology. Cell physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 84 citations in OpenAlex.
- Severe Muscle Deconditioning Triggers Early Extracellular Matrix Remodeling and Resident Stem Cell Differentiation into Adipocytes in Healthy Men.International journal of molecular sciences · 2022Trial
- Integrin-β1/FAK signaling is involved in electrical stimulation to prevent disuse muscular atrophy induced by tail suspension in mice.BMC musculoskeletal disorders · 2026Article
- Tenascin-C orchestrates radiotherapy-induced head and neck tumor regression.EMBO molecular medicine · 2026Article
- Muscle transcriptome profiling reveals novel molecular pathways and biomarkers in laminin-α2 deficient patients.Acta neuropathologica communications · 2026Article
- Filamented Light (FLight) Bioprinting of Mini-Muscles with Self-Renewal Potential.Advanced materials (Deerfield Beach, Fla.) · 2025Article
- Extracellular matrix in skeletal muscle injury and atrophy: mechanisms and therapeutic implications.Journal of orthopaedic translation · 2025Review
- Passive hydrotherapy preserves cartilage and muscle integrity in a murine osteoarthritis model: potential role of integrin αV/TGF-β mechanotransduction.Frontiers in physiology · 2025Article
- Resistance exercise: a mighty tool that adapts, destroys, rebuilds and modulates the molecular and structural environment of skeletal muscle.Physical activity and nutrition · 2023Article
- RNA sequencing analysis revealed differentially expressed genes and their functional annotation in porcineFrontiers in veterinary science · 2023Article
- Proteomic Identification of Markers of Membrane Repair, Regeneration and Fibrosis in the Aged and Dystrophic Diaphragm.Life (Basel, Switzerland) · 2022Article
- TMEM182 interacts with integrin beta 1 and regulates myoblast differentiation and muscle regeneration.Journal of cachexia, sarcopenia and muscle · 2021Article
- Lateral rectus muscle differentiation potential in paralytic esotropia patients.BMC ophthalmology · 2021Article
- Laminin and Integrin in LAMA2-Related Congenital Muscular Dystrophy: From Disease to Therapeutics.Frontiers in molecular neuroscience · 2020Article
- Thrombospondin-3 augments injury-induced cardiomyopathy by intracellular integrin inhibition and sarcolemmal instability.Nature communications · 2019Article
- Loss of mouse cardiomyocyte talin-1 and talin-2 leads to β-1 integrin reduction, costameric instability, and dilated cardiomyopathy.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Engineered matrices for skeletal muscle satellite cell engraftment and function.Matrix biology : journal of the International Society for Matrix Biology · 2017Review
- SU9516 Increases α7β1 Integrin and Ameliorates Disease Progression in the mdx Mouse Model of Duchenne Muscular Dystrophy.Molecular therapy : the journal of the American Society of Gene Therapy · 2017Article
- αAmerican journal of physiology. Cell physiology · 2017Article
- PTRH2 gene mutation causes progressive congenital skeletal muscle pathology.Human molecular genetics · 2017Article
- Development and Growth of the Avian Pectoralis Major (Breast) Muscle: Function of Syndecan-4 and Glypican-1 in Adult Myoblast Proliferation and Differentiation.Frontiers in physiology · 2017Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The dystrophin-glycoprotein complex maintains the integrity of skeletal muscle by associating laminin in the extracellular matrix with the actin cytoskeleton. Several human muscular dystrophies arise from defects in the components of this complex. The alpha(7)beta(1)-integrin also binds laminin and links the extracellular matrix with the cytoskeleton. Enhancement of alpha(7)-integrin levels alleviates pathology in mdx/utrn(-/-) mice, a model of Duchenne muscular dystrophy, and thus the integrin may functionally compensate for the absence of dystrophin. To test whether increasing alpha(7)-integrin levels affects transcription and cellular functions, we generated alpha(7)-integrin-inducible C2C12 cells and transgenic mice that overexpress the integrin in skeletal muscle. C2C12 myoblasts with elevated levels of integrin exhibited increased adhesion to laminin, faster proliferation when serum was limited, resistance to staurosporine-induced apoptosis, and normal differentiation. Transgenic expression of eightfold more integrin in skeletal muscle did not result in notable toxic effects in vivo. Moreover, high levels of alpha(7)-integrin in both myoblasts and in skeletal muscle did not disrupt global gene expression profiles. Thus increasing integrin levels can compensate for defects in the extracellular matrix and cytoskeleton linkage caused by compromises in the dystrophin-glycoprotein complex without triggering apparent overt negative side effects. These results support the use of integrin enhancement as a therapy for muscular dystrophy.
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Registered trials
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