ArticleMolecular therapy : the journal of the American Society of Gene Therapy2011
Blocking the myostatin signal with a dominant negative receptor improves the success of human myoblast transplantation in dystrophic mice.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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20 citing papers in PubMed, 41 citations in OpenAlex.
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- The Effect of MSTN Mutation on Bile Acid Metabolism and Lipid Metabolism in Cattle.Metabolites · 2023Article
- Skeletal muscle cell transplantation: models and methods.Journal of muscle research and cell motility · 2020Article
- Peptide-2 from mouse myostatin precursor protein alleviates muscle wasting in cancer-associated cachexia.Cancer science · 2020Article
- Satellite cells and their regulation in livestock.Journal of animal science · 2020Review
- Muscle Hyperplasia in Japanese Quail by Single Amino Acid Deletion in MSTN Propeptide.International journal of molecular sciences · 2020Article
- Identification and Characterization of Long Noncoding RNAs in Ovine Skeletal Muscle.Animals : an open access journal from MDPI · 2018Article
- Follistatin N terminus differentially regulates muscle size and fat in vivo.Experimental & molecular medicine · 2017Article
- Neuromuscular electrical stimulation promotes development in mice of mature human muscle from immortalized human myoblasts.Skeletal muscle · 2016Article
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- Pharmacology of manipulating lean body mass.Clinical and experimental pharmacology & physiology · 2015Review
- Knockdown of endogenous myostatin promotes sheep myoblast proliferation.In vitro cellular & developmental biology. Animal · 2014Article
- Recent progress in satellite cell/myoblast engraftment -- relevance for therapy.The FEBS journal · 2013Review
- Effect of the myostatin locus on muscle mass and intramuscular fat content in a cross between mouse lines selected for hypermuscularity.BMC genomics · 2013Article
- An image analysis method for the precise selection and quantitation of fluorescently labeled cellular constituents: application to the measurement of human muscle cells in culture.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2012Article
- Administration of a soluble activin type IIB receptor promotes the transplantation of human myoblasts in dystrophic mice.Cell transplantation · 2012Article
- Optimization of Xenografting Methods for Generating Human Skeletal Muscle in Mice.Cell transplantationArticle
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3 authors at 1 institution in 1 country.
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Abstract
Duchenne muscular dystrophy (DMD) is a recessive disease caused by a dystrophin gene mutation. Myoblast transplantation permits to introduce the dystrophin gene in dystrophic muscle fibers. However, the success of this approach is reduced by the short duration of the regeneration following the transplantation, which reduces the number of hybrid fibers. Myostatin (MSTN) is a negative regulator of skeletal muscle development and responsible for limiting regeneration. It binds with high affinity to the activin type IIB receptor (ActRIIB). Our aim was to verify whether the success of the myoblast transplantation is enhanced by blocking the MSTN signal with expression of a dominant negative mutant of ActRIIB (dnActRIIB). In vitro, blocking MSTN activity with a lentivirus carrying dnActRIIB increased proliferation and fusion of human myoblasts because MSTN regulates the expression of several myogenic regulatory factors. In vivo, myoblasts infected with the dnActRIIB lentivirus were transplanted in immunodeficient dystrophic mice. Dystrophin immunostaining of tibialis anterior (TA) cross-sections of these mice 1 month post-transplantation revealed more human dystrophin-positive myofibers following the transplantation of dnActRIIB myoblasts than of control myoblasts. Thus, blocking the MSTN signal with dnActRIIB improved the success of myoblast transplantation by increasing the myoblast proliferation and fusion and changed the expression of myogenic regulatory factors.
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