TLR2 deficiency attenuates skeletal muscle atrophy in mice

Kim, Dae-Sung; Cha, Hye-Na; Jo, Hye Jun; Song, In‐Hwan; Baek, Suk‐Hwan; Dan, Jinmyoung; Kim, Yong-Woon; Kim, Jong-Yeon; Lee, Inkyu; Seo, Jae-Sung; Park, Soyoung

doi:10.1016/j.bbrc.2015.02.144

Cited by 25 publications

(23 citation statements)

References 43 publications

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“…Importantly, Kim et al reported that the mRNA levels of inflammatory cytokines increase in atrophied muscle 14 days after cast immobilization. 15 However, skeletal muscle pro-inflammatory cytokine levels during the early stages of atrophy after cast immobilization are unknown. Herein we observed that TNF-a and IL-1b mRNA levels were increased in skeletal muscle at 7 and 14 days after cast immobilization.…”

Section: Discussionmentioning

confidence: 99%

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Time‐course study of macrophage infiltration and inflammation in cast immobilization–induced atrophied muscle of mice

2018

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Section: Discussionmentioning

confidence: 99%

“…13,14 Kim et al reported that mRNA levels of inflammatory cytokines were increased in skeletal muscle after 14 days of cast immobilization. 15 Thus, cast immobilization2induced elevation of inflammatory cytokines may play an important role in the development of skeletal muscle atrophy.…”

mentioning

confidence: 99%

Time‐course study of macrophage infiltration and inflammation in cast immobilization–induced atrophied muscle of mice

2018

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“…To generate muscle and atrophy models, we adopted the procedure described by Kim et al (29). In brief, 100 μl of 10 μM cardiotoxin (CTX) was injected into the left gastrocnemius muscle and PBS was injected into the contralateral gastrocnemius muscle as the control.…”

Section: Methodsmentioning

confidence: 99%

Fibromodulin: a master regulator of myostatin controlling progression of satellite cells through a myogenic program

et al. 2016

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Differentiation of muscle satellite cells (MSCs) involves interaction of the proteins present in the extracellular matrix (ECM) with MSCs to regulate their activity, and therefore phenotype. Herein, we report fibromodulin (FMOD), a member of the proteoglycan family participating in the assembly of ECM, as a novel regulator of myostatin (MSTN) during myoblast differentiation. In addition to having a pronounced effect on the expression of myogenic marker genes [myogenin (MYOG) and myosin light chain 2 (MYL2)], FMOD was found to maintain the transcriptional activity of MSTN Moreover, coimmunoprecipitation and in silico studies performed to investigate the interaction of FMOD helped confirm that it antagonizes MSTN function by distorting its folding and preventing its binding to activin receptor type IIB. Furthermore, in vivo studies revealed that FMOD plays an active role in healing by increasing satellite cell recruitment to sites of injury. Together, these findings disclose a hitherto unrecognized regulatory role for FMOD in MSCs and highlight new mechanisms whereby FMOD circumvents the inhibitory effects of MSTN and triggers myoblast differentiation. These findings offer a basis for the design of novel MSTN inhibitors that promote muscle regeneration after injury or for the development of pharmaceutical agents for the treatment of different muscle atrophies.-Lee, E. J., Jan, A. T., Baig, M. H., Ashraf, J. M., Nahm, S.-S., Kim, Y.-W., Park, S.-Y., Choi, I. Fibromodulin: a master regulator of myostatin controlling progression of satellite cells through a myogenic program.

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“…The muscle injury model was produced as described by Kim et al (24). Briefly, mice were anesthetized with avertin, and 100 μl of 10 μM cardiotoxin (CTX) was injected into the gastrocnemius muscle.…”

Section: Methodsmentioning

confidence: 99%

“…All experimental procedures were performed in accordance with the guidelines issued by the Institutional Animal Care and Use Committees of the Catholic University of Daegu (IACUC-2014-035), and by Yeungnam University (AEC2012-004). The muscle injury model was produced as described by Kim et al (24). Briefly, mice were anesthetized with avertin, and 100 ml of 10 mM cardiotoxin (CTX) was injected into the gastrocnemius muscle.…”

Section: Mouse Studiesmentioning

confidence: 99%

Fibromodulin and regulation of the intricate balance between myoblast differentiation to myocytes or adipocyte‐like cells

et al. 2018

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Interactions between myoblasts and the surrounding microenvironment led us to explore the role of fibromodulin (FMOD), an extracellular matrix protein, in the maintenance of myoblast stemness and function. Microarray analysis of FMOD kd myoblasts and in silico studies were used to identify the top most differentially expressed genes in FMOD kd , and helped establish that FMOD-based regulations of integral membrane protein 2a and clusterin are essential components of the myogenic program. Studies in knockout, obese, and diabetic mouse models helped characterize the operation of a novel FMOD-based regulatory circuit that controls myoblast switching from a myogenic to a lipid accumulation fate. FMOD regulation of myoblasts is an essential part of the myogenic program, and it offers opportunities for the development of therapeutics for the treatment of different muscle

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TLR2 deficiency attenuates skeletal muscle atrophy in mice

Cited by 25 publications

References 43 publications

Time‐course study of macrophage infiltration and inflammation in cast immobilization–induced atrophied muscle of mice

Time‐course study of macrophage infiltration and inflammation in cast immobilization–induced atrophied muscle of mice

Fibromodulin: a master regulator of myostatin controlling progression of satellite cells through a myogenic program

Fibromodulin and regulation of the intricate balance between myoblast differentiation to myocytes or adipocyte‐like cells

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