Ontology highlight
ABSTRACT:
PROVIDER: PRJNA951946 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24060475_1.fastq.gz | Fastqsanger.gz | |||
| SRR24060475_2.fastq.gz | Fastqsanger.gz | |||
| SRR24060476_1.fastq.gz | Fastqsanger.gz | |||
| SRR24060476_2.fastq.gz | Fastqsanger.gz | |||
| SRR24060477_1.fastq.gz | Fastqsanger.gz |
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Project description:Gut microbiota dysbiosis-mediated ceramides elevation contributes to corticosterone-induced depression by impairing mitochondrial function
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Project description:Background: As a worldwide threat to mental health, depression affects about 322 million people globally. Recently, the role of gut microbiota dysbiosis on the pathogenesis of depression has received widespread attention, but the underlying mechanism remains elusive.Results: Corticosterone (CORT)-treated mice showed depressive-like behaviors, a reduction in hippocampal neurogenesis, and an altered composition of gut microbiota (GM). Fecal microbial transplantation (FMT) from CORT-treated mice transferred depressive-like phenotypes and their dominant GM, especially bifidobacterium and lactobacillus, to the recipients. Fecal metabolic profiling showed that the relative abundances of fecal ceramides were significantly increased in CORT-treated and the recipient mice. Metagenomic sequencing exposed that bifidobacterium and lactobacillus might be responsible for gut ceramides production in CORT-treated mice. We then found that treatment with ceramides via oral gavage was sufficient to recapitulate the depressive-like phenotypes in wild -type mice. Finally, RNA-sequencing data exposed that most of the differentially expressed genes (DEGs) between ceramides-treated mice and the control group were enriched in oxidative phosphorylation (OXPHOS) pathway. Conclusion: We conclude that chronic exposure to CORT leads to an altered GM composition and consequent ceramides production, thus leading to subtle mitochondrial OXPHOS dysfunction in hippocampus, which may contribute to the development of depressive disorders.
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Project description:Animal models represent a very useful tool for the study of depressive-like behaviour and for the evaluation of the therapeutic efficacy of antidepressants. Nevertheless, gene expression patterns of these different animal models and whether genes classically associated to human major depression are present in these genetic profiles remain unknown. Gene expression was evaluated in an animal model of depression: corticosterone-treated rats. Gene expression analyses were carried out using the Affymetrix® GeneChip® technology. Experiment Overall Design: In total, 19 animals were studied, 10 corticosterone-treated rats and 9 control rats
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Project description:Environmental changes may alter gene expression in depression and anxiety disorders through epigenetic regulation, including small non-coding RNAs (sncRNAs) and their major subclass, microRNAs (miRNAs). However, underlying mechanisms mediating miRNA regulation in response to changing environmental stimuli are unclear. Using the serotonin transporter (5-HTT) knockout (KO) mouse model of depression/anxiety, this study aimed to compare the effects of voluntary exercise versus chronic treatment with the stress hormone, corticosterone, on miRNA transcriptome and proteome. Using high-throughput sequencing of miRNAs and mass spectrometry (MS)-based approaches for protein expression, we described 337 differentially expressed (DE) miRNAs and 67 proteins in 5-HTT KO mice compared to wild-type (WT) control mice in standard-housing conditions. After exercise, there were 200 DE miRNAs and 3 DE proteins in WT mice, and 20 DE miRNAs and 95 DE proteins in 5-HTT KO mice, while corticosterone treatment led to 168 DE miRNAs and 1 DE protein in WT, and 21 DE miRNAs and 21 DE proteins in 5-HTT KO mice. Serotonergic dysfunction (due to the 5-HTT KO gene mutation) induced altered expression of miRNAs and proteins involved in regulation of neurodevelopment, neurogenesis and neuroinflammatory responses. Elevation of the stress hormone corticosterone activated similar (to 5-HTT KO) molecules in WT mice, while exercise caused antidepressant-like effects. We suggest that these findings indicate that functional 5-HTT might be required for the beneficial effects of exercise on miRNA expression. Our study is the first to explore how gene-environment interactions affect miRNA/proteomics composition in a mouse model of depression/anxiety and extends our understanding of gene-environmental interactions underlying these affective disorders.
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Project description:Analysis of mRNA gene expression changes mediated by natural glucocorticoid ligand corticosterone in mouse cortical primary astrocyte cultures; also, parallel analysis of RU486 (mifepristone) antagonism of corticosterone-mediated mRNA changes. Total RNA obtained from astrocyte cultures subjected to 2, 4, or 6 hours of (1) 100nM corticosterone alone, (2) 500nM RU486 alone, or (3) 100nM corticosterone + 500nM RU486 exposure compared to vehicle control astrocyte cultures.
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Project description:The severe harm of depression to human life has attracted great attention to neurologists, but its pathogenesis is extremely complicated and has not yet been fully elaborated. Here, we provided a new strategy for revealing the specific pathways of abnormal brain glucose catabolism in depression, which from the supply of energy substrates and the evaluation of mitochondrial structure and function. By using stable isotope-resolved metabolomics technique, we discovered the tricarboxylic acid cycle (TCA cycle) is blocked and the gluconeogenesis is abnormally activated in chronic unpredictable mild stress (CUMS) rats. In addition, our results showed an interesting phenomenon that the brain attempted to activate all possible metabolic enzymes in energy-producing pathways, but CUMS rats still exhibited a low TCA cycle activity due to impaired mitochondria. Depression caused mitochondrial structure and function impaired, and then led to abnormal brain glucose catabolism. The combination of the stable isotope-resolved metabolomics and mitochondrial structure and function analysis can accurately clarify the mechanism of depression. The mitochondrial pyruvate carrier and acetyl-CoA maybe the key targets for depression treatment. The strategy provides a unique insight for exploring the mechanism of depression, the discovery of new targets, and the development of ideal novel antidepressants.
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