Mouse gut metagenome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA454894 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7120950.fastq.gz | Fastqsanger.gz | |||
| SRR7120950_1.fastq.gz | Fastqsanger.gz | |||
| SRR7120950_2.fastq.gz | Fastqsanger.gz | |||
| SRR7120960.fastq.gz | Fastqsanger.gz | |||
| SRR7120960_1.fastq.gz | Fastqsanger.gz |
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Project description:Induced pluripotent stem cell (iPSC)-derived dopamine neurons provide an opportunity to model Parkinson’s disease (PD) but neuronal cultures are confounded by cellular heterogeneity. By applying high-resolution single cell transcriptomic analyses to Parkinson’s iPSC-derived dopamine neurons carrying the GBA-N370S risk variant, we exploited intra-culture cellular heterogeneity to identify a progressive axis of gene expression variation leading to endoplasmic reticulum stress. Analysis of genes differentially-expressed (DE) along this axis identified the transcriptional repressor histone deacetylase 4 (HDAC4) as an upstream regulator of disease progression. HDAC4 was mislocalized to the nucleus in PD iPSC-derived dopamine neurons and repressed genes early in the disease axis, leading to late deficits in protein homeostasis. Treatment of iPSC-derived dopamine neurons with compounds known to modulate HDAC4 activity upregulated genes early in the DE axis, and corrected Parkinson’s-related cellular phenotypes. Our study demonstrates how single cell transcriptomics can exploit cellular heterogeneity to reveal disease mechanisms and identify therapeutic targets.
2018-10-17 | E-MTAB-7303 | biostudies-arrayexpress
Project description:To uncover new disease-associated genes and their relevant mechanisms, we carried out a gene microarray analysis based on a Parkinson’s disease (PD) in vitro model induced by a-synuclein oligomers. The result do help to reveal the mRNA and lncRNA profile in a-syn induced cells and rotenone-stimulated cells.
2018-09-28 | GSE120569 | GEO
Project description:Mitochondrial dysfunction plays a major role in the pathogenesis of sporadic Parkinson’s disease (PD) and familial PD caused by mutations in the PARK2 gene. The protein, parkin, is vital for mitochondrial function, but the lack of key PD phenotypes in PARK2 knockout (KO) rodent models has hindered investigations into parkin’s role in PD pathogenesis. Human isogenic induced pluripotent stem cell (iPSC) lines with and without PARK2 KO enable studies of the effect of parkin dysfunction in dopaminergic neuronal cultures.
2019-07-26 | PXD008894 | Pride
Project description:Mitochondrial dysfunction plays a major role in the pathogenesis of sporadic Parkinson’s disease (PD) and familial PD caused by mutations in the PARK2 gene. The protein, parkin, is vital for mitochondrial function, but the lack of key PD phenotypes in PARK2 knockout (KO) rodent models has hindered investigations into parkin’s role in PD pathogenesis. Human isogenic induced pluripotent stem cell (iPSC) lines with and without PARK2 KO enable studies of the effect of parkin dysfunction in dopaminergic neuronal cultures.
2019-09-03 | PXD007871 | Pride
Project description:Rotenone is a neurotoxic substance that inhibits mitochondrial respiratory chain complex I, decreases ATP production and increases oxidative stress. It exhibits neurotoxic effects, particularly on dopamine-producing neurons, and is associated with the etiology of Parkinson’s disease. To better understand the impact of rotenone on neural development and function, we examined the effect of rotenone on gene expression using human induced pluripotent stem (iPS) cells-derived neural organoids. Cells were treated with rotenone as well as the controls at varying concentrations (0.3 μM, 1 μM, and 25 μM) for 48 hours. RNA was subsequently extracted, and RNA sequencing (RNA-seq) was performed to analyze gene expression profiles. The results revealed that rotenone exposure potentially suppresses critical ligand-receptor interactions involved in neural development. Network interaction analysis of KEGG signaling pathways highlighted the involvement of the focal adhesion pathway and the neuroactive ligand-receptor interaction pathway in the neurotoxic effects of rotenone.
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Project description:Background: The long-term high-fat, high-sugar diet exacerbates type 2 diabetes mellitus (T2DM)-related cognitive impairments. The negative impact of poor dietary patterns on brain development and neurological function may be related to gut microbiota disturbance. The role of phlorizin in mitigating glucose and lipid metabolism disorders is well documented. However, the protective effect of phlorizin on diabetes-related cognitive dysfunction is unclear. Therefore, the present study aimed to investigate the effect of dietary supplementation of phlorizin on high-fat and high-fructose diet (HFFD)-induced cognitive dysfunction and evaluate the crucial role of the microbiota-gut-brain axis. Results: Dietary supplementation of phlorizin for 14 weeks effectively prevented glucolipid metabolism disorder, spatial learning impairment, and memory impairment in HFFD mice. In addition, phlorizin improved the HFFD-induced decrease in synaptic plasticity, neuroinflammation, and excessive activation of microglia in the hippocampus. Transcriptomics analysis shows that the protective effect of phlorizin on cognitive impairment was associated with increased expression of neurotransmitters and synapse-related genes in the hippocampus. Phlorizin treatment alleviated colon microbiota disturbance, mainly manifested by an increase in gut microbiota diversity and the abundance of short-chain fatty acid (SCFA)-producing bacteria. The level of microbial metabolites, including SCFA, inosine 5'-monophosphate (IMP), and D (-)-beta-hydroxybutyric acid (BHB) were also significantly increased after phlorizin treatment. Moreover, integrating multiomics analysis observed tight connections between phlorizin-regulated genes, microbiota, and metabolites. Furthermore, removal of the gut microbiota via antibiotics treatment diminished the protective effect of phlorizin against HFFD-induced cognitive impairment, underscoring the critical role of the gut microbiota in mediating cognitive behavior. Importantly, supplementation with SCFA and BHB alone mimicked the regulatory effects of phlorizin on cognitive function. Conclusions: These results indicate that gut microbiota and their metabolites mediate the ameliorative effect of phlorizin on HFFD-induced cognitive impairment. Therefore, phlorizin can be used as an easy-to-implement nutritional therapy to prevent and alleviate metabolism-related neurodegenerative diseases by targeting the regulation of the microbiome-gut-brain axis.
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Project description:The lack of knowledge about the onset and progression of Parkinson’s disease (PD) hampers its early diagnosis and treatment. We used a multiplatform untargeted metabolomics-based approach to uncover the biochemical remodeling induced by PD in a really early and pre-symptomatic stage and unveiling early potential diagnostic biomarkers. Baseline pre-clinical plasma samples (Pre-PD n=39; control group n=39) were obtained from the European Prospective Study on Nutrition and Cancer (EPIC) cohort, which healthy volunteers were followed for around 15 years to ascertain incident PD. Our finding revealed alterations in fatty acids metabolism, mitochondrial dysfunction, oxidative stress, and gut-brain axis dysregulation. This study is of inestimable value since this is the first study conducted with samples collected many years before the disease development.
2021-06-01 | ST001814 | MetabolomicsWorkbench
Project description:The pesticide rotenone, a neurotoxin that inhibits the mitochondrial complex I, and destabilizes microtubules (MT) has been linked to Parkinson disease (PD) etiology and is often used to model this neurodegenerative disease (ND). Many of the mechanisms of action of rotenone are posited mechanisms of neurodegeneration; however, they are not fully understood. Therefore, the study of rotenone-affected functional pathways is pertinent to the understanding of NDs pathogenesis. This report describes the transcriptome analysis of a neuroblastoma (NB) cell line chronically exposed to marginally toxic and moderately toxic doses of rotenone. The results revealed a complex pleiotropic response to rotenone that impacts a variety of cellular events, including cell cycle, DNA damage response, proliferation, differentiation, senescence and cell death, which could lead to survival or neurodegeneration depending on the dose and time of exposure and cell phenotype. The response encompasses an array of physiological pathways, modulated by transcriptional and epigenetic regulatory networks, likely activated by homeostatic alterations. Pathways that incorporate the contribution of MT destabilization to rotenone toxicity are suggested to explain complex I-independent rotenone-induced alterations of metabolism and redox homeostasis. The postulated mechanisms involve the blockage of mitochondrial voltage-dependent anions channels (VDACs) by tubulin, which coupled with other rotenone-induced organelle dysfunctions may underlie many presumed neurodegeneration mechanisms associated with pathophysiological aspects of various NDs including PD, AD and their variant forms. Thus, further investigation of such pathways may help identify novel therapeutic paths for these NDs.
2012-08-09 | GSE35642 | GEO
Project description:Peripheral autonomic nervous system (P-ANS) dysfunction is a critical non-motor phenotype of Parkinson's disease (PD). While the majority of PD cases are sporadic with no identified PD-associated genes involved, epidemiological and animal model studies suggest an association with pesticides and other environmental toxins but underlying cellular mechanisms affecting the human P-ANS is unclear. Here, we mapped the global transcriptome changes in human induced-pluripotent stem cell (iPSC) derived P-ANS sympathetic neurons followed by exposure to the PD-related pesticide, rotenone. Surprisingly, we revealed distinct transcriptome profiles between acute and chronic exposure to rotenone. In the acute stage, there was a down regulation of specific cation channel genes mediating action potential signaling, while in the chronic stage, the human P-ANS neurons exhibited dysregulation of anti-apoptotic and Golgi apparatus-related pathways. Moreover, we identified the sodium voltage-gated channel subunit SCN3A/Nav1.3 as a potential biomarker in human P-ANS neurons associated with PD. Our analysis of the rotenone-altered coding and non-coding genome of human P-ANS neurons may thus provide insight into the pathological signaling events that occur in the sympathetic neurons during PD progression.
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Project description:Parkinson's disease (PD) is a common neurodegenerative disease in middle-aged and elderly people. The disorder of gut microbiota is involved in the pathophysiological process of various neurological diseases, and many studies have confirmed that gut microbiota is involved in the progression of PD. As one of the most effective methods to reconstruct gut microbiota, fecal microbiota transplantation (FMT) has been considered as an important treatment for PD. However, the mechanism of FMT treatment for PD is still lacking, which requires further exploration and can facilitate the application of FMT. As a model organism, Drosophila is highly conserved with mammalian system in maintaining intestinal homeostasis. In this study, there were significant differences in the gut microbiota of conventional Drosophila colonized from PD patients compared to those transplanted from normal controls. And we constructed rotenone-induced PD model in Drosophila followed by FMT in different groups, and investigated the impact of gut microbiome on transcriptome of the PD host. Microbial analysis by 16S rDNA sequencing showed that gut microbiota could affect bacterial structure of PD, which was confirmed by bacterial colonization results. In addition, transcriptome data suggested that gut microbiota can influence gene expression pattern of PD. Further experimental validations confirmed that lysosome and neuroactive ligand-receptor interaction are the most significantly influenced functional pathways by PD-derived gut microbiota. In summary, our data reveals the influence of PD-derived gut microbiota on host transcriptome and helps better understanding the interaction between gut microbiota and PD through gut-brain axis. The present study will facilitate the understanding of the mechanism underlying PD treatment with FMT in clinical practice.
2023-01-13 | GSE221760 | GEO