Chronic stress targets mitochondrial respiratory efficiency in the skeletal muscle of C57BL/6 mice
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ABSTRACT:
PROVIDER: PRJNA865927 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR20822466_1.fastq.gz | Fastqsanger.gz | |||
| SRR20822466_2.fastq.gz | Fastqsanger.gz | |||
| SRR20822467_1.fastq.gz | Fastqsanger.gz | |||
| SRR20822467_2.fastq.gz | Fastqsanger.gz | |||
| SRR20822468_1.fastq.gz | Fastqsanger.gz |
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Project description:Episodes of chronic stress can result in psychic disorders like post-traumatic stress disorder, but also promote the development of metabolic syndrome and type 2 diabetes. We hypothesize that muscle, as main regulator of whole-body energy expenditure, is a central target of acute and adaptive molecular effects of stress in this context. Here, we investigate the immediate effect of a stress period on energy metabolism in Musculus gastrocnemius in our established C57BL/6 chronic variable stress (Cvs) mouse model. Cvs decreased lean body mass despite increased energy intake, reduced circadian energy expenditure (EE), and substrate utilization. Cvs altered the proteome of metabolic components but not of the oxidative phosphorylation system (OXPHOS), or other mitochondrial structural components. Functionally, Cvs impaired the electron transport chain (ETC) capacity of complex I and complex II, and reduces respiratory capacity of the ETC from complex I to ATP synthase. Complex I-OXPHOS correlated to diurnal EE and complex II-maximal uncoupled respiration correlated to diurnal and reduced nocturnal EE. Bioenergetics assessment revealed higher optimal thermodynamic efficiencies (ƞ-opt) of mitochondria via complex II after Cvs. Interestingly, transcriptome and methylome were unaffected by Cvs, thus excluding major contributions to supposed metabolic adaptation processes. In summary, the preclinical Cvs model shows that metabolic pressure by Cvs is initially compensated by adaptation of mitochondria function associated with high thermodynamic efficiency and decreased EE to manage the energy balance. This counter-regulation of mitochondrial complex II may be the driving force to longitudinal metabolic changes of muscle physiological adaptation as the basis of stress memory.Chronic stress targets mitochondrial respiratory efficiency in the skeletal muscle of C57BL/6 mice.Nikolic A, Fahlbusch P, Wahlers N, Riffelmann NK, Jacob S, Hartwig S, Kettel U, Dille M, Al-Hasani H, Kotzka J, Knebel B. Cell Mol Life Sci. 2023 Mar 29;80(4):108. doi: 10.1007/s00018-023-04761-4.PMID: 36988756
2024-03-08 | PXD042472 | Pride
Project description:Chronic stress targets mitochondrial respiratory efficiency in the skeletal muscle of C57BL/6 mice [Methylome Dataset]
| PRJNA865930 | ENA
Project description:Chronic stress targets mitochondrial respiratory efficiency in the skeletal muscle of C57BL/6 mice [Transcriptome Dataset]
| PRJNA865365 | ENA
Project description:Episodes of chronic stress can result in psychic disorders like post-traumatic stress disorder, but also promote the development of metabolic syndrome and type 2 diabetes. We hypothesize that muscle, as main regulator of whole-body energy expenditure, is a central target of acute and adaptive molecular effects of stress in this context. Here, we investigate the immediate effect of a stress period on energy metabolism in Musculus gastrocnemius in our established C57BL/6 chronic variable stress (Cvs) mouse model. Cvs decreased lean body mass despite increased energy intake, reduced circadian energy expenditure (EE), and substrate utilization. Cvs altered the proteome of metabolic components but not of the oxidative phosphorylation system (OXPHOS), or other mitochondrial structural components. Functionally, Cvs impaired the electron transport chain (ETC) capacity of complex I and complex II, and reduces respiratory capacity of the ETC from complex I to ATP synthase. Complex I-OXPHOS correlated to diurnal EE and complex II-maximal uncoupled respiration correlated to diurnal and reduced nocturnal EE. Bioenergetics assessment revealed higher optimal thermodynamic efficiencies (ƞ-opt) of mitochondria via complex II after Cvs. Interestingly, transcriptome and methylome were unaffected by Cvs, thus excluding major contributions to supposed metabolic adaptation processes. In summary, the preclinical Cvs model shows that metabolic pressure by Cvs is initially compensated by adaptation of mitochondria function associated with high thermodynamic efficiency and decreased EE to manage the energy balance. This counter-regulation of mitochondrial complex II may be the driving force to longitudinal metabolic changes of muscle physiological adaptation as the basis of stress memory.
2023-04-03 | GSE210365 | GEO
Project description:Episodes of chronic stress can result in psychic disorders like post-traumatic stress disorder, but also promote the development of metabolic syndrome and type 2 diabetes. We hypothesize that muscle, as main regulator of whole-body energy expenditure, is a central target of acute and adaptive molecular efects of stress in this context. Here, we investigate the immediate efect of a stress period on energy metabolism in Musculus gastrocnemius in our established C57BL/6 chronic variable stress (Cvs) mouse model. Cvs decreased lean body mass despite increased energy intake, reduced circadian energy expenditure (EE), and substrate utilization. Cvs altered the proteome of metabolic components but not of the oxidative phosphorylation system (OXPHOS), or other mitochondrial structural components. Functionally, Cvs impaired the electron transport chain (ETC) capacity of complex I and complex II, and reduces respiratory capacity of the ETC from complex I to ATP synthase. Complex I-OXPHOS correlated to diurnal EE and complex II-maximal uncoupled respiration correlated to diurnal and reduced nocturnal EE. Bioenergetics assessment revealed higher optimal thermodynamic efciencies (ƞ-opt) of mitochondria via complex II after Cvs. Interestingly, transcriptome and methylome were unafected by Cvs, thus excluding major contributions to supposed metabolic adaptation processes. In summary, the preclinical Cvs model shows that metabolic pressure by Cvs is initially compensated by adaptation of mitochondria function associated with high thermodynamic efciency and decreased EE to manage the energy balance. This counter-regulation of mitochondrial complex II may be the driving force to longitudinal metabolic changes of muscle physiological adaptation as the basis of stress memory.
2023-03-31 | PXD035798 | Pride
Project description:Chronic stress can result in dysregulation of the cellular metabolism leading to severe disorders including depression, posttraumatic stress disorder but also the metabolic syndrome and type 2 diabetes. We aimed to determine the acute and adaptive effect of stress on energy metabolism in muscle tissue as the main determinant of whole-body energy expenditure. C57Bl6 mice under 15 days of chronic variable stress (Cvs) showed decreased lean mass despite increased energy intake. This was accompanied by reduced energy expenditure (EE) with a concomitant shift in substrate utilization depending on the circadian rhythm. The combination of omics approaches excluded stress effects on transcription and methylation processes in gastrocnemius muscle. Nevertheless, Cvs interfered with altered proteome composition in mitochondria on metabolic components, whilst OXPHOS and structural relevant components were unaltered. Functionally, Cvs resulted in impaired complex independent mitochondrial electron flow and reduced coupling efficiency that correlate for oxidative phosphorylation (state 3) of complex I to diurnal energy expenditure (EE) and for maximal uncoupled respiration (state 3u) of complex II to reduced diurnal and nocturnal EE. Bioenergetics assessment of mitochondria revealed higher optimal thermodynamic efficiencies (ƞ-opt) in Cvs muscle. Conclusion: These results show, that the Cvs reduced mitochondria respiration is associate with low rate of total EE, but does not primary affect transcription and genome methylation in muscle. However, the counter regulation by increased efficiency of complex II may be the driving force in to pave the way to longitudinal metabolic changes as basis of stress memory to muscle physiological adaptation.
2023-04-03 | GSE210509 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2023-04-03 | GSE210510 | GEO
Project description:Chronic stress alters hepatic metabolism and thermodynamic respiratory efficiency affecting epigenetics in C57BL/6 mice
| PRJNA986046 | ENA
Project description:Respiratory supercomplexes provide metabolic efficiency in zebrafish
| PRJNA551601 | ENA
Project description:Primary mitochondrial respiratory chain (RC) diseases are heterogeneous in etiology and manifestations but collectively impair cellular energy metabolism. To identify a common cellular response to RC disease, systems biology level transcriptome investigations were performed in human RC disease skeletal muscle and fibroblasts. Global transcriptional and post-transcriptional dysregulation in a tissue-specific fashion was identified across diverse RC complex and genetic etiologies. RC disease muscle was characterized by decreased transcription of cytosolic ribosomal proteins to reduce energy-intensive anabolic processes, increased transcription of mitochondrial ribosomal proteins, shortened 5'-UTRs to improve translational efficiency, and stabilization of 3'-UTRs containing AU-rich elements. These same modifications in a reversed direction typified RC disease fibroblasts. RC disease also dysregulated transcriptional networks related to basic nutrient-sensing signaling pathways, which collectively mediate many aspects of tissue-specific cellular responses to primary RC disease. These findings support the utility of a systems biology approach to improve mechanistic understanding of mitochondrial RC disease. To identify a common cellular response to primary RC that might improve mechanistic understanding and lead to targeted therapies for human RC disease, we performed collective transcriptome profiling in skeletal muscle biopsy specimens and fibroblast cell lines (FCLs) of a diverse cohort of human mitochondrial disease subjects relative to controls. Systems biology investigations of common cellular responses to primary RC disease revealed a collective pattern of transcriptional, post-transcriptional and translational dysregulation occurring in a highly tissue-specific fashion. Affymetrix Human Exon 1.0ST microarray analysis was performed on 29 skeletal muscle samples and Fibroblast cell lines from mitochondrial disease patients and age- and gender-matched controls.
2013-07-01 | E-GEOD-42986 | biostudies-arrayexpress