Genome-wide identification of enhancer domains in the healthy and post-stroke mouse cortices
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ABSTRACT:
PROVIDER: PRJNA559075 | ENA |
REPOSITORIES: ENA
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Project description:We report the identification of enhancer domains in sham and stroke mouse cerebral cortices by high-throughput profiling of H3K27Ac chromatin modification. A total of 35.4, 28.8 and 29.6 million reads were generated from chromatin immunoprecipitated DNA from sham, stroke and pooled input samples. This resulted in 55,571 peaks in sham and 56,110 peaks in stroke samples representing 50408 and 51,292 active regions, respectively. These active regions represent putative enhancer domains.
2020-11-12 | GSE135480 | GEO
Project description:RNA-sequencing was conducted to profile the transcriptome of the eRNA_06347 knockdown post-stroke mouse cortices ( knockdown achieved by intracerebroventricular injection of oligos against eRNA_06347). RNA was isolated from sham, Negative control oligo injected post-stroke cortices and eRNA_06347 knockown post-stroke cortices (three independent biological replicates per group),converted into cDNA libraries, and used for Illumina deep sequencing.The sequencing reads were aligned to the mouse reference genome GRCm38 using HISAT2. Stringtie was used to assemble the aligned sequences into transcript isoforms using mouse transcript annotations from Ensembl 81 as a guide, then merged to reconstruct a comprehensive transcriptome using perl scripts and gffcompare. After the final transcriptome was generated, StringTie and Ballgown were used to estimate the expression levels of all the transcripts. StringTie was used to evaluate expression levels for mRNAs by calculating the FPKMs. The differentially expressed mRNAs were identified as log2 fold change >1 or log2 fold change <-1 and with statistical significance p<0.05 using Ballgown.Doing so, We found that 106 genes were significantly upregulated and 49 genes were significantly downregulated in the eRNA_06347 knockdown group as compared to the negative control.
2020-11-12 | GSE136405 | GEO
Project description:We conducted bulk RNA sequencing on infarcts collected from young adult (3-month-old) mice at 7 weeks after the distal middle cerebral artery occlusion + hypoxia stroke model and compared them to contralateral cortices. As expected, differential expression (DE) analysis revealed marked differences between infarcts and contralateral cortices: 3,930 upregulated and 2,869 downregulated genes. The most significantly upregulated genes, including Lpl, Spp1, Cd36, Mmp2, and Mmp19, and the most highly enriched genes, including Cd5l, Mmp3, Mmp12, and Mmp13, indicate a pronounced disturbance in lipid homeostasis in infarcts at 7 weeks after stroke. In addition to alterations in lipid metabolic processes, the transcriptome also revealed a signature of chronic inflammation at 7 weeks after stroke. We then used IPA software to define upstream regulators and identify altered biological processes based on DE analysis. Differentially expressed genes were associated with the following upregulated biological processes: (i) atherosclerosis signaling, (ii) IL-1 signaling, (iii) inflammasome pathway, (iv) eicosanoid signaling, (v) B cell receptor (BCR) signaling, and (vi) phospholipases, along with others. IPA also identified lipid metabolic upstream regulators such as cholesterol, phospholipids, and LDL, as well as immunological upstream regulators such as MYD88, IL18, CD3, IL1B, TLR4, and TNF. These altered biological processes indicate that the stroke infarct transcriptome is characterized by chronic inflammation, dysregulated lipid metabolism, and impaired or absent neuronal function at 7 weeks after stroke.
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Project description:RNA Sequencing of WT Chronic Stroke Infarcts vs. Contralateral Cortices
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Project description:After ischemic stroke, the brain initiates intensive communication with the immune system, and acetylcholine contributes to this process. Stroke triggers peripheral immunosuppression leading to increased susceptibility to infections; and post-stroke pneumonia is linked with poor stroke outcome, but the responsible processes are yet unknown. We discovered a “change of guards” where microRNA levels decreased but small transfer RNA fragments (tRFs) accumulated in post-stroke blood cells. This molecular switch may re-balance acetylcholine signaling in CD14+ monocytes by regulating their gene expression and modulating post-stroke immunity. Our observations point to tRFs as new molecular regulators of post-stroke immune responses that may become potential therapeutic targets.
2020-12-31 | GSE158312 | GEO
Project description:After ischemic stroke, the brain initiates intensive communication with the immune system, and acetylcholine contributes to this process. Stroke triggers peripheral immunosuppression leading to increased susceptibility to infections; and post-stroke pneumonia is linked with poor stroke outcome, but the responsible processes are yet unknown. We discovered a “change of guards” where microRNA levels decreased but small transfer RNA fragments (tRFs) accumulated in post-stroke blood cells. This molecular switch may re-balance acetylcholine signaling in CD14+ monocytes by regulating their gene expression and modulating post-stroke immunity. Our observations point to tRFs as new molecular regulators of post-stroke immune responses that may become potential therapeutic targets.
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Project description:After ischemic stroke, the brain initiates intensive communication with the immune system, and acetylcholine contributes to this process. Stroke triggers peripheral immunosuppression leading to increased susceptibility to infections; and post-stroke pneumonia is linked with poor stroke outcome, but the responsible processes are yet unknown. We discovered a “change of guards” where microRNA levels decreased but small transfer RNA fragments (tRFs) accumulated in post-stroke blood cells. This molecular switch may re-balance acetylcholine signaling in CD14+ monocytes by regulating their gene expression and modulating post-stroke immunity. Our observations point to tRFs as new molecular regulators of post-stroke immune responses that may become potential therapeutic targets.
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Project description:CD8 T cells functional profile was characterized by comparing the gene expression between the cells isolated from 3 days post-stroke, 30 days post-stroke and naïve brains.
2020-11-01 | GSE155480 | GEO
Project description:Stroke is a prevalent disorder representing the third leading cause of death and major cause of disability. Post-stroke epilepsy (PSE) has been recognized as a common clinical issue after stroke, accounting for 30-40% of the causes of epilepsy among older adults. In this study, we determined GABAA receptor-mediated seizure susceptibility after PT cerebral stroke in aged mice. Young adult mice around 10 weeks of age are widely used in stroke experiments. However, as most strokes are diagnosed in the elderly and PSE has been recognized as a common clinical incidence after stroke, we utilized photothrombosis (PT) model of cerebral ischemia and examined seizure susceptibility and brain injury using combined behavioral (video) and EEG monitoring and histological (MRI) assessments. To investigate GABAA receptor-mediated convulsive/non-convulsive seizures, lower-doses of pentylenetetrazol (PTZ) was injected. PTZ susceptibility in aging mice increased compared to young adults. One month after PT stroke, aged PT stroke mice exhibited severe convulsive seizures (late-onset). These findings exhibited the increase of GABAA receptor-mediated seizures susceptibility in PT stroke aging mice, but not in young adults.
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Project description:This transcriptomic study investigates the effect of therapeutic short-chain fatty acids (SCFA) administration on post-stroke recovery.
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