Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1030992 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26465700_1.fastq.gz | Fastqsanger.gz | |||
| SRR26465700_2.fastq.gz | Fastqsanger.gz | |||
| SRR26465701_1.fastq.gz | Fastqsanger.gz | |||
| SRR26465701_2.fastq.gz | Fastqsanger.gz | |||
| SRR26465702_1.fastq.gz | Fastqsanger.gz |
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Project description:To explore the effects of gut microbiota of young (8 weeks) or old mice (18～20 months) on stroke, feces of young (Y1-Y9) and old mice (O6-O16) were collected and analyzed by 16s rRNA sequencing. Then stroke model was established on young mouse receive feces from old mouse (DOT1-15) and young mouse receive feces from young mouse (DYT1-15). 16s rRNA sequencing were also performed for those young mice received feces from young and old mice.
2021-10-15 | E-MTAB-10837 | biostudies-arrayexpress
Project description:Intracerebral hemorrhage (ICH) induces alterations in the gut microbiota composition, significantly impacting neuroinflammation post-ICH. However, the impact of gut microbiota absence on neuroinflammation following ICH-induced brain injury remain unexplored. Here, we observed that the gut microbiota absence was associated with reduced neuroinflammation, alleviated neurological dysfunction, and mitigated gut barrier dysfunction post-ICH. In contrast, recolonization of microbiota from ICH-induced SPF mice by transplantation of fecal microbiota (FMT) exacerbated brain injury and gut impairment post-ICH. Additionally, microglia with transcriptional changes mediated the protective effects of gut microbiota absence on brain injury, with Apoe emerging as a hub gene. Subsequently, Apoe deficiency in peri-hematomal microglia was associated with improved brain injury. Finally, we revealed that gut microbiota influence brain injury and gut impairment via gut-derived short-chain fatty acids (SCFA).
2024-05-13 | GSE266602 | GEO
Project description:Neurogenesis after stroke compounded with amyloid beta plaques around the cerebral vasculature has implications in delaying tissue recovery. We used single cell RNA sequencing (scRNA-seq) to understand the cellular interactions in the hippocampus during post-stroke recovery with CAA.
2024-05-26 | GSE266033 | GEO
Project description:Post-stroke recovery is an ongoing process as the brain attempts to reverse or minimize ischemia- induced disturbances in multiple biological systems. Currently, the longitudinal profile of molecular changes in patients post-stroke is relatively unknown. We therefore aimed to characterise biological pathways in plasma involved in post-stroke recovery using a discovery proteomics workflow coupled with a topological pathway systems biology approach. Blood samples (n = 180, EDTA plasma) were taken from a subgroup of 60 first episode stroke survivors from the Australian START cohort over 3 timepoints: 3-7 days (T1), 3-months (T2) and 12-months (T3) post primary event . Samples were analysed by liquid chromatography mass spectrometry (LC-MS) on the Q Exactive HF hybrid quadrupole-Orbitrap (Thermo-Fisher Scientific) using label-free quantification. The proteomics results were analysed for differential expression of all identified proteins for all available pairwise time-point comparisons. The resulting significant lists of proteins were then submitted for Gene Graph Enrichment Analysis (GGEA).
2020-08-31 | PXD015006 | Pride
Project description:Background: The etiology of Inflammatory Bowel Disease (IBD) is unclear but involves both genetics and environmental factors, including the gut microbiota. Indeed, exacerbated activation of the gastrointestinal immune system toward the gut microbiota occurs in genetically susceptible hosts and under the influence of the environment. For instance, a majority of IBD susceptibility loci lie within genes involved in immune responses, such as caspase recruitment domain member 9 (Card9). However, the relative impacts of genotype versus microbiota on colitis susceptibility in the context of CARD9 deficiency remain unknown. Results: Card9 gene directly contributes to recovery from dextran sodium sulfate (DSS)-induced colitis by inducing the colonic expression of the cytokine IL-22 and the antimicrobial peptides Reg3 and Reg3 independently of the microbiota. On the other hand, Card9 is required for regulating the microbiota capacity to produce AhR ligands, which leads to the production of IL-22 in the colon, promoting recovery after colitis. In addition, cross-fostering experiments showed that five weeks after weaning, the microbiota transmitted from the nursing mother before weaning had a stronger impact on the tryptophan metabolism of the pups than the pups' own genotype. Conclusions: These results show the role of CARD9 and its effector IL-22 in mediating recovery from DSS-induced colitis in both microbiota-independent and microbiota-dependent manners. Card9 genotype modulates the microbiota metabolic capacity to produce AhR ligands, but this effect can be overridden by the implantation of a WT or healthy microbiota before weaning. It highlights the importance of the weaning reaction occurring between the immune system and microbiota for the host metabolism and immune functions throughout life. A better understanding of the impact of genetics on microbiota metabolism is key to developing efficient therapeutic strategies for patients suffering from complex inflammatory disorders.
2024-05-01 | GSE262585 | GEO
Project description:This transcriptomic study investigates the effect of therapeutic short-chain fatty acids (SCFA) administration on post-stroke recovery.
2020-01-01 | GSE131788 | GEO
Project description:Neutrophils, key players in the innate immune system, become activated following ischemic stroke. However, the influence of gut microbiota on neutrophil activation and its impact on inflammatory brain injury is not yet fully understood. In this study, we demonstrate that microbiota colonization in germ-free mice activates neutrophils and worsens disease outcomes. To investigate the phenotypic and molecular alterations in neutrophils, as well as their activity in stroke mice with either depleted or intact microbiota, we conducted a comparative proteomic analysis using liquid chromatography-based mass spectrometry. Our findings revealed that microbiota depletion leads to a downregulation of inflammatory proteins in circulating neutrophils and a reduction in neutrophil extracellular traps (NETs). A similar pattern was observed in neutrophils infiltrating the brain, accompanied by a decrease in infarct size and alleviated behavioral deficits.
2025-06-02 | PXD060229 | Pride
Project description:In response to cortical stroke and unilateral corticospinal tract degeneration, compensatory sprouting of spared corticospinal fibers is associated with recovery of skilled movement in rodents. To date, little is known about the molecular mechanisms orchestrating this spontaneous rewiring. In this study, we provide insights into the molecular changes in the spinal cord tissue after large ischemic cortical injury in adult female mice, with a focus on factors that might influence the re-innervation process by contralesional corticospinal neurons. We mapped the area of cervical grey matter re-innervation by sprouting contralesional corticospinal axons after unilateral photothrombotic stroke of the motor cortex in mice using anterograde tracing. The mRNA profile of this re-innervation area was analyzed using whole-genome sequencing to identify differentially expressed genes at selected time points during the recovery process. Bioinformatic analysis revealed two phases of processes: Early after stroke (4-7 days post injury), the spinal transcriptome is characterized by inflammatory processes, including phagocytic processes as well as complement cascade activation. Microglia are specifically activated in the denervated corticospinal projection fields in this early phase. In a later phase (28-42 days post injury), biological processes include tissue repair pathways with up-regulated genes related to neurite outgrowth. Thus, the stroke-denervated spinal grey matter, in particular its intermediate laminae, represents a growth-promoting environment for sprouting corticospinal fibers originating from the contralesional motor cortex. This data set provides a solid starting point for future studies addressing key elements of the post-stroke recovery process, with the goal to improve neuroregenerative treatment options for stroke patients.
2019-04-30 | GSE128623 | GEO
Project description:Prospective cohort studies and meta-analyses examining the relationship between HDL-cholesterol (C) and stroke risk are discordant and question the value of HDL-C as a marker for stroke risk prediction. However, the relationship between other metrics of HDL, function and proteome, and stroke remain unexplored. We investigated changes in HDL protein composition and function -cholesterol efflux capacity (CEC)- after acute ischemic stroke, and their relationship to long-term functional and neuronal recovery after stroke. Plasma samples were collected from healthy controls (N = 35) and from stroke patients either 24 (early, N = 35) or 96 hours (late, N = 20) after stroke onset. ABCA1 mediated CEC was measured using murine macrophages. Stroke recovery was assessed at 3 months after stroke event using the Modified Rankin Scores (MRS) and the NIH Stroke Scale (NIHSS). Proteomic analysis of HDL by parallel reaction monitoring indicated a distinct time-dependent remodeling after stroke. 15 proteins were significantly altered following stroke, with 6 proteins significantly changing between 24 and 96 h post stroke. Inflammation-related proteins (SAA1, SAA2, PON1) were increased at both time points. Macrophage CEC, consistent with inflammatory remodeling of HDL proteome, was reduced by 50% (P<0.0001) in both early and late post-stroke samples compared to the controls. Changes in 6 post-stroke significantly correlated with stroke recovery scores (P<0.05). Further, the multiple linear regression model adjusting for baseline stroke severity confirmed that these proteins that predict the stroke recovery. Changes in HDL associated proteins within the first 96 hours post stroke could be used as markers to predict functional stroke recovery.
2021-01-24 | PXD015001 | panorama