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         headline:Androgen-dependent impairment of myogenesis in spinal and bulbar muscular atrophy
         description:Spinal and bulbar muscular atrophy (SBMA) is an inherited neuromuscular disease caused by expansion of a polyglutamine (polyQ) tract in the androgen receptor (AR). SBMA is triggered by the interaction between polyQ-AR and its natural ligands, testosterone and dihydrotestosterone (DHT). SBMA is characterized by the loss of lower motor neurons and skeletal muscle fasciculations, weakness, and atrophy. To test the hypothesis that the interaction between polyQ-AR and androgens exerts cell-autonomous toxicity in skeletal muscle, we characterized the process of myogenesis and polyQ-AR expression in DHT-treated satellite cells obtained from SBMA patients and age-matched healthy control subjects. Treatment with androgens increased the size and number of myonuclei in myotubes from control subjects, but not from SBMA patients. Myotubes from SBMA patients had a reduced number of nuclei, suggesting impaired myotube fusion and altered contractile structures. The lack of anabolic effects of androgens on myotubes from SBMA patients was not due to defects in myoblast proliferation, differentiation or apoptosis. DHT treatment of myotubes from SBMA patients increased nuclear accumulation of polyQ-AR and decreased the expression of interleukin-4 (IL-4) when compared to myotubes from control subjects. Following DHT treatment, exposure of myotubes from SBMA patients with IL-4 treatment rescued myonuclear number and size to control levels. This supports the hypothesis that androgens alter the fusion process in SBMA myogenesis. In conclusion, these results provide evidence of an androgen-dependent impairment of myogenesis in SBMA that could contribute to disease pathogenesis.
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      headline:Androgen-dependent impairment of myogenesis in spinal and bulbar muscular atrophy
      description:Spinal and bulbar muscular atrophy (SBMA) is an inherited neuromuscular disease caused by expansion of a polyglutamine (polyQ) tract in the androgen receptor (AR). SBMA is triggered by the interaction between polyQ-AR and its natural ligands, testosterone and dihydrotestosterone (DHT). SBMA is characterized by the loss of lower motor neurons and skeletal muscle fasciculations, weakness, and atrophy. To test the hypothesis that the interaction between polyQ-AR and androgens exerts cell-autonomous toxicity in skeletal muscle, we characterized the process of myogenesis and polyQ-AR expression in DHT-treated satellite cells obtained from SBMA patients and age-matched healthy control subjects. Treatment with androgens increased the size and number of myonuclei in myotubes from control subjects, but not from SBMA patients. Myotubes from SBMA patients had a reduced number of nuclei, suggesting impaired myotube fusion and altered contractile structures. The lack of anabolic effects of androgens on myotubes from SBMA patients was not due to defects in myoblast proliferation, differentiation or apoptosis. DHT treatment of myotubes from SBMA patients increased nuclear accumulation of polyQ-AR and decreased the expression of interleukin-4 (IL-4) when compared to myotubes from control subjects. Following DHT treatment, exposure of myotubes from SBMA patients with IL-4 treatment rescued myonuclear number and size to control levels. This supports the hypothesis that androgens alter the fusion process in SBMA myogenesis. In conclusion, these results provide evidence of an androgen-dependent impairment of myogenesis in SBMA that could contribute to disease pathogenesis.
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         Androgen receptor
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      email:[email protected]
PostalAddress:
      name:Department of Neuroscience SNPSRR, University of Padova, Padova, Italy
      name:Department of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia, Genoa, Italy
      name:Department of Neuroscience SNPSRR, University of Padova, Padova, Italy
      name:Department of Neuroscience SNPSRR, University of Padova, Padova, Italy
      name:Department of Neuroscience SNPSRR, University of Padova, Padova, Italy
      name:IRCCS Istituto Auxologico Italiano, Milan, Italy
      name:Department of Radiological and Histocytopathological Sciences, University of Bologna, Bologna, Italy
      name:Department of Radiological and Histocytopathological Sciences, University of Bologna, Bologna, Italy
      name:Neurology Unit, Verona Hospital, Verona, Italy
      name:Neurological Institute C. Besta, Milan, Italy
      name:Department of Neuroscience SNPSRR, University of Padova, Padova, Italy
      name:Aaron Russell, Center for Physical Activity and Nutrition Research, School of Exercise and Nutrition Sciences, Deakin University, Burwood, Australia
      name:Department of Neuroscience SNPSRR, University of Padova, Padova, Italy
      name:Department of Neuroscience SNPSRR, University of Padova, Padova, Italy
      name:Centro Biomedico Pietro D’Abano-via Orus 2, Padova, Italy
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• What's the monthly income of https://www.springernature.com/?

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