The health-promoting effects of regular exercise are well known, and myokines may mediate some of these effects. The small leucine-rich proteoglycan decorin has been described as a myokine for some time. However, its regulation and impact on skeletal muscle has not been investigated in detail. In this study, we report decorin to be differentially expressed and released in response to muscle contraction using different approaches. Decorin is released from contracting human myotubes, and circulating decorin levels are increased in response to acute resistance exercise in humans. Moreover, decorin expression in skeletal muscle is increased in humans and mice after chronic training. Because decorin directly binds myostatin, a potent inhibitor of muscle growth, we investigated a potential function of decorin in the regulation of skeletal muscle growth. In vivo overexpression of decorin in murine skeletal muscle promoted expression of the pro-myogenic factor Mighty, which is negatively regulated by myostatin. We also found Myod1 and follistatin to be increased in response to decorin overexpression. Moreover, muscle-specific ubiquitin ligases atrogin1 and MuRF1, which are involved in atrophic pathways, were reduced by decorin overexpression. In summary, our findings suggest that decorin secreted from myotubes in response to exercise is involved in the regulation of muscle hypertrophy and hence could play a role in exercise-related restructuring processes of skeletal muscle.

3rd Faculty of Medicine Charles University Prague Czech Republic

Department of Experimental Diabetology German Institute of Human Nutrition Potsdam Rehbrücke Germany

Department of Nutrition Institute for Basic Medical Sciences University of Oslo Oslo Norway

Department of Physical Performance Norwegian School of Sport Sciences Oslo Norway

German Center for Diabetes Research Germany

Paul Langerhans Group for Integrative Physiology German Diabetes Center Düsseldorf Germany

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$a Kanzleiter, Timo $u Department of Experimental Diabetology, German Institute of Human Nutrition, Potsdam-Rehbrücke, Germany; German Center for Diabetes Research, Germany.

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$a The myokine decorin is regulated by contraction and involved in muscle hypertrophy / $c T. Kanzleiter, M. Rath, SW. Görgens, J. Jensen, DS. Tangen, AJ. Kolnes, KJ. Kolnes, S. Lee, J. Eckel, A. Schürmann, K. Eckardt,

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$a The health-promoting effects of regular exercise are well known, and myokines may mediate some of these effects. The small leucine-rich proteoglycan decorin has been described as a myokine for some time. However, its regulation and impact on skeletal muscle has not been investigated in detail. In this study, we report decorin to be differentially expressed and released in response to muscle contraction using different approaches. Decorin is released from contracting human myotubes, and circulating decorin levels are increased in response to acute resistance exercise in humans. Moreover, decorin expression in skeletal muscle is increased in humans and mice after chronic training. Because decorin directly binds myostatin, a potent inhibitor of muscle growth, we investigated a potential function of decorin in the regulation of skeletal muscle growth. In vivo overexpression of decorin in murine skeletal muscle promoted expression of the pro-myogenic factor Mighty, which is negatively regulated by myostatin. We also found Myod1 and follistatin to be increased in response to decorin overexpression. Moreover, muscle-specific ubiquitin ligases atrogin1 and MuRF1, which are involved in atrophic pathways, were reduced by decorin overexpression. In summary, our findings suggest that decorin secreted from myotubes in response to exercise is involved in the regulation of muscle hypertrophy and hence could play a role in exercise-related restructuring processes of skeletal muscle.

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$a Rath, Michaela $u Department of Experimental Diabetology, German Institute of Human Nutrition, Potsdam-Rehbrücke, Germany; German Center for Diabetes Research, Germany.

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$a Görgens, Sven W $u German Center for Diabetes Research, Germany; Paul-Langerhans-Group for Integrative Physiology, German Diabetes Center, Düsseldorf, Germany.

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$a Jensen, Jørgen $u Department of Physical Performance, Norwegian School of Sport Sciences, Oslo, Norway.

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$a Tangen, Daniel S $u Department of Physical Performance, Norwegian School of Sport Sciences, Oslo, Norway.

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$a Kolnes, Anders J $u Third Faculty of Medicine, Charles University, Prague, Czech Republic.

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$a Kolnes, Kristoffer J $u Department of Physical Performance, Norwegian School of Sport Sciences, Oslo, Norway; Third Faculty of Medicine, Charles University, Prague, Czech Republic.

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$a Lee, Sindre $u Department of Nutrition, Institute for Basic Medical Sciences, University of Oslo, Oslo, Norway.

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$a Eckel, Jürgen $u German Center for Diabetes Research, Germany; Paul-Langerhans-Group for Integrative Physiology, German Diabetes Center, Düsseldorf, Germany.

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$a Schürmann, Annette $u Department of Experimental Diabetology, German Institute of Human Nutrition, Potsdam-Rehbrücke, Germany; German Center for Diabetes Research, Germany.

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$a Eckardt, Kristin $u German Center for Diabetes Research, Germany; Paul-Langerhans-Group for Integrative Physiology, German Diabetes Center, Düsseldorf, Germany; Department of Nutrition, Institute for Basic Medical Sciences, University of Oslo, Oslo, Norway. Electronic address: Kristin.Eckardt@medisin.uio.no.

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