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:Perturbations in proximal tubule mitochondrial function and lipid metabolism potentiate kidney dysfunction in acute kidney injury (AKI). We identified the bioactive lipid ceramides as drivers of proximal tubule pathology in AKI. Ceramide synthesis was upregulated in humans and mice with AKI. We utilized a proteome-wide thermal shift assay to observe that ceramides interact with proximal tubule proteins involved in lipid and mitochondrial metabolism. Mechanistic studies revealed that ceramides altered assembly of the inner mitochondrial membrane MICOS complex and respiratory supercomplexes in proximal tubule cells leading to acute impacts on mitochondrial respiration, cristae architecture, and mitochondrial morphology. Effects of ceramides on complex assembly and mitochondrial function were dependent on the presence of the 4-5 trans double bond incorporated by dihydroceramide desaturase 1 (DES1). Blunting ceramide synthesis, via genetic or pharmacologic inhibition of DES1, prevented kidney injury in mice following renal ischemia reperfusion injury. Ceramides may be a novel therapeutic target to combat mitochondrial disruption during AKI.
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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:Dengue virus non-structural protein 3 inhibits mitochondrial respiration by impairing complex I function
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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:Periodontitis is increasingly linked to diverse brain disorders, yet causal mechanisms remain elusive. Here we demonstrate that ligature-induced oral dysbiosis in mice is sufficient to perturb central function. Six weeks of periodontitis produced anxiety-like behavior and motor deficits, accompanied by microglial depletion, reduced neuronal activity and region-selective transcriptional down-regulation in the frontal cortex. Pharmacological microglial ablation phenocopied, and glucocorticoid-receptor blockade rescued, these abnormalities, implicating microglia and activation of the hypothalamic–pituitary–adrenal axis. 16S rRNA gene sequencing revealed significant shifts in oral and gut microbiota that were partially normalized by a broad-spectrum antibiotic cocktail. Antibiotics alone elevated corticosterone but did not affect microglia or behavior, indicating that dysbiosis and glucocorticoids act synergistically on the brain dysfunction. Antibiotic treatment restored microglial density and behaviors in ligature mice, despite plasma corticosterone levels remaining elevated and comparable to those in antibiotic-treated controls. Our findings suggest oral dysbiosis as a tractable driver of neuroimmune dysfunction and redefine periodontitis as a systemic disorder with direct consequences for brain health.
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Project description:Periodontitis is increasingly linked to diverse brain disorders, yet causal mechanisms remain elusive. Here we demonstrate that ligature-induced oral dysbiosis in mice is sufficient to perturb central function. Six weeks of periodontitis produced anxiety-like behavior and motor deficits, accompanied by microglial depletion, reduced neuronal activity and region-selective transcriptional down-regulation in the frontal cortex. Pharmacological microglial ablation phenocopied, and glucocorticoid-receptor blockade rescued, these abnormalities, implicating microglia and activation of the hypothalamic–pituitary–adrenal axis. 16S rRNA gene sequencing revealed significant shifts in oral and gut microbiota that were partially normalized by a broad-spectrum antibiotic cocktail. Antibiotics alone elevated corticosterone but did not affect microglia or behavior, indicating that dysbiosis and glucocorticoids act synergistically on the brain dysfunction. Antibiotic treatment restored microglial density and behaviors in ligature mice, despite plasma corticosterone levels remaining elevated and comparable to those in antibiotic-treated controls. Our findings suggest oral dysbiosis as a tractable driver of neuroimmune dysfunction and redefine periodontitis as a systemic disorder with direct consequences for brain health.
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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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