CHCHD4-TRIAP1 regulation of innate immune signaling mediates skeletal muscle adaptation to exercise
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1029906 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26436300_1.fastq.gz | Fastqsanger.gz | |||
| SRR26436300_2.fastq.gz | Fastqsanger.gz | |||
| SRR26436301_1.fastq.gz | Fastqsanger.gz | |||
| SRR26436301_2.fastq.gz | Fastqsanger.gz | |||
| SRR26436302_1.fastq.gz | Fastqsanger.gz |
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Project description:Exercise training can stimulate the formation of fatty acid oxidizing slow-twitch skeletal muscle fibers which are inversely correlated with obesity, but the molecular mechanism underlying this transformation requires further elucidation. Here, we report that the downregulation of the mitochondrial disulfide relay carrier CHCHD4 in skeletal muscle by exercise training decreases the import of TP53-regulated inhibitor of apoptosis 1 (TRIAP1) into mitochondria, which reduces cardiolipin levels and promotes VDAC oligomerization. The subsequent release of mtDNA into the cytosol activates innate immune signaling through cGAS and NFKB, downregulating MyoD and promoting the formation of oxidative slow-twitch fibers. In mice, CHCHD4 haploinsufficiency was sufficient to activate this pathway, leading to increased oxidative muscle fibers and decreased fat accumulation with aging. The identification of a specific mediator regulating muscle fiber transformation provides an opportunity to understand further the molecular underpinnings of complex metabolic conditions such as obesity and could have therapeutic implications.
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Project description:The skeletal muscle interstitial space is the extracellular region around myofibres and mediates crosstalk between resident cell types. We applied a proteomic workflow to characterise the human skeletal muscle interstitial fluid proteome at rest and in response to exercise. Following exhaustive exercise, markers of skeletal muscle damage accumulate in the interstitial space followed in turn by the appearance of immune cell-derived proteins. Among the proteins upregulated after exercise, we identified cathelicidin-related antimicrobial peptide (CAMP) as a bioactive molecule regulating muscle fibre development. Treatment with the bioactive peptide derivative of CAMP (LL-37) resulted in the growth of larger C2C12 skeletal muscle myotubes. Phosphoproteomics revealed that LL-37 activated pathways central to muscle growth and proliferation, including PI3K, AKT, MAPKs, and mTOR. Our findings provide a proof-of-concept that the interstitial fluid proteome can be quantified via microdialysis sampling in vivo. Furthermore, these data highlight the importance of cellular communication in the adaptive response to exercise.
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Project description:The few investigations on exercise-induced global gene expression responses in human skeletal muscle haves typically focused at one specific mode of exercise and few such studies have implemented control measures. However, interpretation on distinct phenotype regulation necessitate comparison between essentially different modes of exercise and the ability to identify true exercise effects, necessitate implementation of independent non-exercise control subjects. Furthermore, muscle transkriptometranscriptome data made available through previous exercise studies can be difficult to extract and interpret by individuals that are inexperienced with bioinformatic procedures. In a comparative study, we; (1) investigated the human skeletal muscle transcriptome response to differentiated exercise and non-exercise control intervention, and; (2) aimed to develop a straightforward search tool to allow for easy extraction and interpretation of our data. We provide a simple spreadsheet containing transcriptome data allowing other investigators to see how mRNA of their interest behave in skeletal muscle following exercise, both endurance, strength and non-exercise. Our approach, allow investigators easy access to information on genuine transcriptome effects of differentiated exercise, to better aid hyporthesis-driven question in this particular field of research.
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Project description:The few investigations on exercise-induced global gene expression responses in human skeletal muscle haves typically focused at one specific mode of exercise and few such studies have implemented control measures. However, interpretation on distinct phenotype regulation necessitate comparison between essentially different modes of exercise and the ability to identify true exercise effects, necessitate implementation of independent non-exercise control subjects. Furthermore, muscle transkriptometranscriptome data made available through previous exercise studies can be difficult to extract and interpret by individuals that are inexperienced with bioinformatic procedures. In a comparative study, we; (1) investigated the human skeletal muscle transcriptome response to differentiated exercise and non-exercise control intervention, and; (2) aimed to develop a straightforward search tool to allow for easy extraction and interpretation of our data. We provide a simple spreadsheet containing transcriptome data allowing other investigators to see how mRNA of their interest behave in skeletal muscle following exercise, both endurance, strength and non-exercise. Our approach, allow investigators easy access to information on genuine transcriptome effects of differentiated exercise, to better aid hyporthesis-driven question in this particular field of research. 18 subjects were divided into 3 groups, performing 12 weeks of Endurance or Strength training or no training. Biopsies for microarray were take before (Pre) and 2½ and 5 hours after the last training session. Isolated RNA from these biopsies were then measured with the Affymetrix Human Gene 1.0 ST arrays.
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