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Effect of MOTS-c treatment on cast immobilization-induced skeletal muscle atrophy

ABSTRACT: Effect of MOTS-c treatment on cast immobilization-induced skeletal muscle atrophy

PROVIDER: PRJNA876924 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21424301.fastq.gz	Fastqsanger.gz
	SRR21424302.fastq.gz	Fastqsanger.gz
	SRR21424303.fastq.gz	Fastqsanger.gz
	SRR21424304.fastq.gz	Fastqsanger.gz
	SRR21424305.fastq.gz	Fastqsanger.gz

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Effect of MOTS-c treatment on cast immobilization-induced skeletal muscle atrophy

Project description:To understand the effect of MOTS-c treatment on cast immobilization-induced skeletal muscle atrophy, we injected MOTS-c into casted mice. We then performed gene expression profiling analysis using data obtained from RNA-seq of three groups: non-immobilization group, immobilization control group, and immobilization and MOTS-c treated group.

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p53 and ATF4 Mediate Distinct and Additive Mechanisms to Skeletal Muscle Atrophy During Limb Immobilization

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p53 and ATF4 Mediate Distinct and Additive Mechanisms to Skeletal Muscle Atrophy During Limb Immobilization

Project description:p53 regulates a distinct subset of skeletal muscle mRNAs during immobilization-induced skeletal muscle atrophy For additional details see Fox et al, p53 and ATF4 mediate distinct and additive pathways to skeletal muscle atrophy during limb immobilization. Am J Physiol Endocrinol Metab. 2014 Aug 1;307(3):E245-61. Bilateral tibialis anterior muscles were harvested at three days for the following conditions: 1) hindlimb immobilization of C57BL/6 mice; 2) hindlimb immobilization of p53 mKO and littermate control mice; 3) transfection of wild type mice with p53 plasmid or control plasmid

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Microarray analysis of mouse skeletal muscle atrophied by a plaster cast

Project description:Muscle atrophy is associated with aging (sarcopenia) and chronic unloading (such as bed confinement and immobilization with casts), as well as various pathological conditions such as type 1 diabetes and nerve injury (denervation). The hindlimb skeletal muscles of C57BL/6 mice (9 weeks old, male) were immobilized (unloaded) by a plaster cast. After 11 days, skeletal muscle was collected and RNA extracted. Expression of Dnmt3a was reduced while expression of Gdf5 was increased by plaster cast immobilization compared to age-matched control mice.

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Expression data from wild type or KLF15 knockout mouse skeletal muscle after immobilization

Project description:Evidence suggests that immobilization is a promoting factor of sarcopenia; mechanism how immobilization accelerates the development of sarcopenia is not known. We have recently established a model of immobilization-induced skeletal muscle mass loss in mice. We used microarrays to detail the global programme of gene expression underlying skeletal muscle atrophy in immobilized mice and identified up-regulated or down-regulated genes during this process.

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Sestrin prevents skeletal muscle atrophy

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The muscle proteome reflects changes in mitochondrial function, cellular stress and proteolysis after 14 days of unilateral lower limb immobilization in active young men

Project description:Skeletal muscle unloading due to joint immobilization induces skeletal muscle atrophy. However, the skeletal muscle proteome response to limb immobilization has not been investigated using SWATH methods. This study quantitatively characterized the muscle proteome at baseline, and after 3 and 14 d of unilateral lower limb (knee-brace) immobilization in 18 healthy young men (25.4 ±5.5 y, 81.2 ±11.6 kg). All muscle biopsies were obtained from the vastus lateralis muscle. Unilateral lower limb immobilization was preceded by four-weeks of exercise training to standardise acute training history, and 7 days of dietary provision to standardise energy/macronutrient intake. Dietary intake was also standardised/provided throughout the 14 d immobilization period.

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Gadd45a Promotes Skeletal Muscle Atrophy by Forming a Complex with the Protein Kinase MEKK4

Project description:Skeletal muscle atrophy is a serious and highly prevalent condition that remains poorly understood at the molecular level. Previous work found that skeletal muscle atrophy involves an increase in skeletal muscle Gadd45a expression, which is necessary and sufficient for skeletal muscle fiber atrophy. However, the direct mechanism by which Gadd45a promotes skeletal muscle atrophy was unknown. To address this question, we biochemically isolated skeletal muscle fiber proteins that associate with Gadd45a as it induces skeletal muscle atrophy in living mice. We found that Gadd45a interacts with multiple proteins in skeletal muscle fibers, including, most prominently, the MAP kinase kinase kinase MEKK4. Furthermore, by forming a complex with MEKK4 in skeletal muscle fibers, Gadd45a increases MEKK4 protein kinase activity, which is sufficient to induce skeletal muscle fiber atrophy and required for Gadd45a-mediated skeletal muscle fiber atrophy. Together, these results identify a direct biochemical mechanism by which Gadd45a induces skeletal muscle atrophy and provide new insight into way that skeletal muscle atrophy occurs at the molecular level.

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Project description:Skeletal muscle atrophy is a highly prevalent and debilitating condition that remains poorly understood at the molecular level. Previous work found that skeletal muscle atrophy involves activating transcription factor 4 (ATF4), a protein in the basic leucine zipper (bZIP) transcription factor family. However, the direct biochemical mechanism by which ATF4 promotes muscle atrophy was unknown. Because bZIP proteins such as ATF4 must dimerize to bind and activate genes, and because ATF4 is unable to form highly stable homodimers, we hypothesized that ATF4 may promote muscle atrophy by heterodimerizing with another bZIP family member. To test this hypothesis, we biochemically isolated skeletal muscle proteins that associate with the dimerization- and DNA-binding domain of ATF4 (the bZIP domain) in mouse skeletal muscle fibers in vivo. Interestingly, we found that ATF4 makes up one half of at least 5 distinct heterodimeric bZIP transcription factors in skeletal muscle fibers. This three-way interaction between ATF4, C/EBPbeta and the ATF4-C/EBP composite site activates the Gadd45a gene, which encodes a known mediator of muscle atrophy (Gadd45a). Together, these results identify a direct biochemical mechanism by which ATF4 induces skeletal muscle atrophy and provide new insight into the way that skeletal muscle atrophy occurs at the molecular level.

2019-11-04 | MSV000084538 | MassIVE

Skeletal muscle-specific DJ-1 ablation-induced atrogenes expression and mitochondrial dysfunction contributing to muscular atrophy

Project description:DJ-1 is a causative gene for a familial form of Parkinson disease. DJ-1 deficient mice develop progressive behavioral abnormalities in gaits and forearm grip strength are hypoactive. The mechanisms under the activity are not fully known. Here we show that DJ-1 is critical for disuse- induced skeletal muscle atrophy. Firstly, DJ-1 expression is positively correlated with muscle mass in human, and is decreased in atrophy muscle of immobilization mice and aged human. Secondly, DJ-1-deficient muscles are dystrophic, as well as impaired in activities and oxidative capacity. In disuse-atrophic condition, skeletal muscle specific-DJ-1 knockout mice show less cross section area (CSA) and more central nuclei than control mice. Thirdly, biochemical analysis indicates that these changes are due to enhanced activation of FoxO1, and subsequent upregulation of atrogenes. Finally, the inhibitor of DJ-1, compound 23, can mimic the effects of DJ-1 ablation in vivo. Our results illuminate that skeletal muscle DJ-1 has an unexpected role in the regulation of catabolic signals from mechanical stimulation, providing a therapeutic target for muscle-wasting diseases.

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