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Lack of the serum- and glucocorticoid-inducible kinase SGK1 improves muscle force characteristics and attenuates fibrosis in dystrophic mdx mouse muscle

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  • Martin Steinberger, Institute of Pathophysiology, University Medicine Greifswald, Unknown
  • Michael Föller, Animal Physiology, Institute for Neurobiology, University of Tübingen, Unknown
  • Silke Vogelgesang, Institute of Pathology, University Medicine Greifswald, Unknown
  • Mirjam Krautwald, Institute of Pathophysiology, University Medicine Greifswald, Unknown
  • Martin Landsberger, Institute of Pathophysiology, University Medicine Greifswald, Unknown
  • Claudia K. Winkler, Institute of Pathophysiology, University Medicine Greifswald, Unknown
  • Joachim Kasch, Institute of Pathophysiology, University Medicine Greifswald, Unknown
  • Ernst Martin Füchtbauer
  • Dietmar Kuhl, The Lundbeck Foundation Research Center MIND, Department of Biomedicine, Aarhus University, Vennelyst Boulevard 4, 8000 C Aarhus, Denmark; Center for Molecular Neurobiology, University Medical Center Hamburg-Eppendorf, 20251 Hamburg, Germany., Germany
  • Jakob Voelkl, Animal Physiology, Institute for Neurobiology, University of Tübingen, Unknown
  • Florian Lang, Animal Physiology, Institute for Neurobiology, University of Tübingen, Germany
  • Heinrich Brinkmeier, Institute of Pathophysiology, University Medicine Greifswald, Unknown
Duchenne muscular dystrophy (DMD) is a human genetic disease characterized by fibrosis and severe muscle weakness. Currently, there is no effective treatment available to prevent progressive fibrosis in skeletal muscles. The serum- and glucocorticoid-inducible kinase SGK1 regulates a variety of physiological functions and participates in fibrosis stimulation. Here, we investigated whether SGK1 influences structure, function and/or fibrosis of the muscles from the mdx mouse, an animal model for DMD. As expected, mdx muscles showed the typical pathological features of muscular dystrophy including fiber size variations, central nuclei of muscle fibers, fibrosis in the diaphragm, and force reduction by 30–50 %. Muscles from sgk1 -/- mice were histologically overall intact and specific force was only slightly reduced compared to wild-type muscles. Surprisingly, soleus and diaphragm muscles of mdx/sgk1 -/- mice displayed forces close to wild-type levels. Most muscle fibers of the double mutants contained central nuclei, but fibrosis was not observed in any of the tested limb and diaphragm muscles. We conclude that the sole lack of SGK1 in mouse muscle does not lead to pronounced changes in muscle structure and function. However, dystrophin-deficient mdx muscle seems to benefit from SGK1 deficiency. SGK1 appears to be an important enzyme in the process of fibrotic remodeling and subsequent weakness of dystrophin-deficient mouse muscle
Original languageEnglish
JournalPflügers Archiv - European Journal of Physiology
Volume1965-1974
Issue10
Pages (from-to)1965-1974
Number of pages10
ISSN0031-6768
DOIs
Publication statusPublished - Sep 2015

    Research areas

  • Fibrosis, mdx, Muscle force, Muscular dystrophy, SGK1

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