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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

Standard

Lack of the serum- and glucocorticoid-inducible kinase SGK1 improves muscle force characteristics and attenuates fibrosis in dystrophic mdx mouse muscle. / Steinberger, Martin; Föller, Michael; Vogelgesang, Silke; Krautwald, Mirjam; Landsberger, Martin; Winkler, Claudia K; Kasch, Joachim; Füchtbauer, Ernst-Martin; Kuhl, Franz-Dietmar; Voelkl, Jakob; Lang, Florian; Brinkmeier, Heinrich.

in: PFLUG ARCH EUR J PHY, Jahrgang 467, Nr. 9, 2015, S. 1065 - 1974.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Steinberger, M, Föller, M, Vogelgesang, S, Krautwald, M, Landsberger, M, Winkler, CK, Kasch, J, Füchtbauer, E-M, Kuhl, F-D, Voelkl, J, Lang, F & Brinkmeier, H 2015, 'Lack of the serum- and glucocorticoid-inducible kinase SGK1 improves muscle force characteristics and attenuates fibrosis in dystrophic mdx mouse muscle', PFLUG ARCH EUR J PHY, Jg. 467, Nr. 9, S. 1065 - 1974. https://doi.org/10.1007/s00424-014-1645-5

APA

Steinberger, M., Föller, M., Vogelgesang, S., Krautwald, M., Landsberger, M., Winkler, C. K., Kasch, J., Füchtbauer, E-M., Kuhl, F-D., Voelkl, J., Lang, F., & Brinkmeier, H. (2015). Lack of the serum- and glucocorticoid-inducible kinase SGK1 improves muscle force characteristics and attenuates fibrosis in dystrophic mdx mouse muscle. PFLUG ARCH EUR J PHY, 467(9), 1065 - 1974. https://doi.org/10.1007/s00424-014-1645-5

Vancouver

Steinberger M, Föller M, Vogelgesang S, Krautwald M, Landsberger M, Winkler CK et al. Lack of the serum- and glucocorticoid-inducible kinase SGK1 improves muscle force characteristics and attenuates fibrosis in dystrophic mdx mouse muscle. PFLUG ARCH EUR J PHY. 2015;467(9):1065 - 1974. https://doi.org/10.1007/s00424-014-1645-5

Bibtex

@article{e169eb44ee5c4f8194610208fe519fe0,
title = "Lack of the serum- and glucocorticoid-inducible kinase SGK1 improves muscle force characteristics and attenuates fibrosis in dystrophic mdx mouse muscle",
abstract = "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.",
author = "Martin Steinberger and Michael F{\"o}ller and Silke Vogelgesang and Mirjam Krautwald and Martin Landsberger and Winkler, {Claudia K} and Joachim Kasch and Ernst-Martin F{\"u}chtbauer and Franz-Dietmar Kuhl and Jakob Voelkl and Florian Lang and Heinrich Brinkmeier",
year = "2015",
doi = "10.1007/s00424-014-1645-5",
language = "English",
volume = "467",
pages = "1065 -- 1974",
journal = "PFLUG ARCH EUR J PHY",
issn = "0031-6768",
publisher = "Springer",
number = "9",

}

RIS

TY - JOUR

T1 - Lack of the serum- and glucocorticoid-inducible kinase SGK1 improves muscle force characteristics and attenuates fibrosis in dystrophic mdx mouse muscle

AU - Steinberger, Martin

AU - Föller, Michael

AU - Vogelgesang, Silke

AU - Krautwald, Mirjam

AU - Landsberger, Martin

AU - Winkler, Claudia K

AU - Kasch, Joachim

AU - Füchtbauer, Ernst-Martin

AU - Kuhl, Franz-Dietmar

AU - Voelkl, Jakob

AU - Lang, Florian

AU - Brinkmeier, Heinrich

PY - 2015

Y1 - 2015

N2 - 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.

AB - 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.

U2 - 10.1007/s00424-014-1645-5

DO - 10.1007/s00424-014-1645-5

M3 - SCORING: Journal article

C2 - 25394886

VL - 467

SP - 1065

EP - 1974

JO - PFLUG ARCH EUR J PHY

JF - PFLUG ARCH EUR J PHY

SN - 0031-6768

IS - 9

ER -