Impaired adaptive response to mechanical overloading in dystrophic skeletal muscle

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Impaired adaptive response to mechanical overloading in dystrophic skeletal muscle. / Joanne, Pierre; Hourdé, Christophe; Ochala, Julien; Caudéran, Yvain; Medja, Fadia; Vignaud, Alban; Mouisel, Etienne; Hadj-Said, Wahiba; Arandel, Ludovic; Garcia, Luis; Goyenvalle, Aurélie; Mounier, Rémi; Zibroba, Daria; Sakamoto, Kei; Sakamato, Kei; Butler-Browne, Gillian; Agbulut, Onnik; Ferry, Arnaud.

I: PLoS ONE, Bind 7, Nr. 4, 2012, s. e35346.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Joanne, P, Hourdé, C, Ochala, J, Caudéran, Y, Medja, F, Vignaud, A, Mouisel, E, Hadj-Said, W, Arandel, L, Garcia, L, Goyenvalle, A, Mounier, R, Zibroba, D, Sakamoto, K, Sakamato, K, Butler-Browne, G, Agbulut, O & Ferry, A 2012, 'Impaired adaptive response to mechanical overloading in dystrophic skeletal muscle', PLoS ONE, bind 7, nr. 4, s. e35346. https://doi.org/10.1371/journal.pone.0035346

APA

Joanne, P., Hourdé, C., Ochala, J., Caudéran, Y., Medja, F., Vignaud, A., Mouisel, E., Hadj-Said, W., Arandel, L., Garcia, L., Goyenvalle, A., Mounier, R., Zibroba, D., Sakamoto, K., Sakamato, K., Butler-Browne, G., Agbulut, O., & Ferry, A. (2012). Impaired adaptive response to mechanical overloading in dystrophic skeletal muscle. PLoS ONE, 7(4), e35346. https://doi.org/10.1371/journal.pone.0035346

Vancouver

Joanne P, Hourdé C, Ochala J, Caudéran Y, Medja F, Vignaud A o.a. Impaired adaptive response to mechanical overloading in dystrophic skeletal muscle. PLoS ONE. 2012;7(4):e35346. https://doi.org/10.1371/journal.pone.0035346

Author

Joanne, Pierre ; Hourdé, Christophe ; Ochala, Julien ; Caudéran, Yvain ; Medja, Fadia ; Vignaud, Alban ; Mouisel, Etienne ; Hadj-Said, Wahiba ; Arandel, Ludovic ; Garcia, Luis ; Goyenvalle, Aurélie ; Mounier, Rémi ; Zibroba, Daria ; Sakamoto, Kei ; Sakamato, Kei ; Butler-Browne, Gillian ; Agbulut, Onnik ; Ferry, Arnaud. / Impaired adaptive response to mechanical overloading in dystrophic skeletal muscle. I: PLoS ONE. 2012 ; Bind 7, Nr. 4. s. e35346.

Bibtex

@article{4424e995b0d5480e83fc0fc573e0fee0,
title = "Impaired adaptive response to mechanical overloading in dystrophic skeletal muscle",
abstract = "Dystrophin contributes to force transmission and has a protein-scaffolding role for a variety of signaling complexes in skeletal muscle. In the present study, we tested the hypothesis that the muscle adaptive response following mechanical overloading (ML) would be decreased in MDX dystrophic muscle lacking dystrophin. We found that the gains in muscle maximal force production and fatigue resistance in response to ML were both reduced in MDX mice as compared to healthy mice. MDX muscle also exhibited decreased cellular and molecular muscle remodeling (hypertrophy and promotion of slower/oxidative fiber type) in response to ML, and altered intracellular signalings involved in muscle growth and maintenance (mTOR, myostatin, follistatin, AMPKα1, REDD1, atrogin-1, Bnip3). Moreover, dystrophin rescue via exon skipping restored the adaptive response to ML. Therefore our results demonstrate that the adaptive response in response to ML is impaired in dystrophic MDX muscle, most likely because of the dystrophin crucial role.",
keywords = "Adaptation, Physiological, Animals, Biomechanical Phenomena, Mice, Muscle Fatigue, Muscle, Skeletal/physiology, Muscular Dystrophy, Duchenne/physiopathology, Signal Transduction",
author = "Pierre Joanne and Christophe Hourd{\'e} and Julien Ochala and Yvain Caud{\'e}ran and Fadia Medja and Alban Vignaud and Etienne Mouisel and Wahiba Hadj-Said and Ludovic Arandel and Luis Garcia and Aur{\'e}lie Goyenvalle and R{\'e}mi Mounier and Daria Zibroba and Kei Sakamoto and Kei Sakamato and Gillian Butler-Browne and Onnik Agbulut and Arnaud Ferry",
year = "2012",
doi = "10.1371/journal.pone.0035346",
language = "English",
volume = "7",
pages = "e35346",
journal = "PLoS ONE",
issn = "1932-6203",
publisher = "Public Library of Science",
number = "4",

}

RIS

TY - JOUR

T1 - Impaired adaptive response to mechanical overloading in dystrophic skeletal muscle

AU - Joanne, Pierre

AU - Hourdé, Christophe

AU - Ochala, Julien

AU - Caudéran, Yvain

AU - Medja, Fadia

AU - Vignaud, Alban

AU - Mouisel, Etienne

AU - Hadj-Said, Wahiba

AU - Arandel, Ludovic

AU - Garcia, Luis

AU - Goyenvalle, Aurélie

AU - Mounier, Rémi

AU - Zibroba, Daria

AU - Sakamoto, Kei

AU - Sakamato, Kei

AU - Butler-Browne, Gillian

AU - Agbulut, Onnik

AU - Ferry, Arnaud

PY - 2012

Y1 - 2012

N2 - Dystrophin contributes to force transmission and has a protein-scaffolding role for a variety of signaling complexes in skeletal muscle. In the present study, we tested the hypothesis that the muscle adaptive response following mechanical overloading (ML) would be decreased in MDX dystrophic muscle lacking dystrophin. We found that the gains in muscle maximal force production and fatigue resistance in response to ML were both reduced in MDX mice as compared to healthy mice. MDX muscle also exhibited decreased cellular and molecular muscle remodeling (hypertrophy and promotion of slower/oxidative fiber type) in response to ML, and altered intracellular signalings involved in muscle growth and maintenance (mTOR, myostatin, follistatin, AMPKα1, REDD1, atrogin-1, Bnip3). Moreover, dystrophin rescue via exon skipping restored the adaptive response to ML. Therefore our results demonstrate that the adaptive response in response to ML is impaired in dystrophic MDX muscle, most likely because of the dystrophin crucial role.

AB - Dystrophin contributes to force transmission and has a protein-scaffolding role for a variety of signaling complexes in skeletal muscle. In the present study, we tested the hypothesis that the muscle adaptive response following mechanical overloading (ML) would be decreased in MDX dystrophic muscle lacking dystrophin. We found that the gains in muscle maximal force production and fatigue resistance in response to ML were both reduced in MDX mice as compared to healthy mice. MDX muscle also exhibited decreased cellular and molecular muscle remodeling (hypertrophy and promotion of slower/oxidative fiber type) in response to ML, and altered intracellular signalings involved in muscle growth and maintenance (mTOR, myostatin, follistatin, AMPKα1, REDD1, atrogin-1, Bnip3). Moreover, dystrophin rescue via exon skipping restored the adaptive response to ML. Therefore our results demonstrate that the adaptive response in response to ML is impaired in dystrophic MDX muscle, most likely because of the dystrophin crucial role.

KW - Adaptation, Physiological

KW - Animals

KW - Biomechanical Phenomena

KW - Mice

KW - Muscle Fatigue

KW - Muscle, Skeletal/physiology

KW - Muscular Dystrophy, Duchenne/physiopathology

KW - Signal Transduction

U2 - 10.1371/journal.pone.0035346

DO - 10.1371/journal.pone.0035346

M3 - Journal article

C2 - 22511986

VL - 7

SP - e35346

JO - PLoS ONE

JF - PLoS ONE

SN - 1932-6203

IS - 4

ER -

ID: 239921042