RNA Sequencing of WT Chronic Stroke Infarcts vs. Contralateral Cortices
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ABSTRACT:
PROVIDER: PRJNA726051 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14355675_1.fastq.gz | Fastqsanger.gz | |||
| SRR14355675_2.fastq.gz | Fastqsanger.gz | |||
| SRR14355676_1.fastq.gz | Fastqsanger.gz | |||
| SRR14355676_2.fastq.gz | Fastqsanger.gz | |||
| SRR14355677_1.fastq.gz | Fastqsanger.gz |
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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: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.
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Project description:We have used microarrays to investigate the changes in gene expression at various times after stroke. Our findings reported that gene expression screening can detect known and unknown transcriptional features of stroke. Brain samples were obtained from 9 patients who died from stroke, with the approval of the local Ethics Committee. The patients were aged between 51 and 86 years and had survived between 2-37 days following stroke. Tissue samples were taken from infarct and peri-infarcted zones while controls were obtained from the contralateral hemisphere. We established mRNA expression profiles of the damaged brain tissues between 2 to 6 days, 9 to 20 days, and 26 to 37 days after stroke. RNA from three stroke patients was pooled for each patient survival group.
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Project description:Prior to assessing the impact of repeated HPβCD administration on the peri-infarct region of the brain, we first compared the transcriptome of the peri-infarct region to the equivalent region of the contralateral hemisphere in aged (18-month-old) mice at 7 weeks after distal middle cerebral artery occlusion + hypoxia (DH) stroke. The peri-infarct region was characterized by 3,910 differentially expressed genes. Of these, 2,123 were upregulated, many of which were also upregulated in infarcts at 7 weeks after stroke. For instance, the infarct and peri-infarct regions were both defined by the upregulation of degradative enzymes, TLRs, and scavenger receptors. In addition, the upregulation of Lpl, Lrp2, Ch25h, Apoe, Trem2, and Abca1 signified a divergence from lipid homeostasis. These alterations in innate immunity coincided with corresponding perturbations in adaptive immunity. The upregulation of Cd3d, Cd3e, Cd3g, Blnk, Sdc1 and Jchain suggests that chronic inflammation persists in peri-infarct regions for at least 7 weeks after stroke. Conversely, the DE analysis revealed that 1,787 genes were downregulated in peri-infarct regions compared to equivalent regions of the contralateral hemisphere. These genes were primarily involved in mitochondrial respiration and neuronal function. Together, these results demonstrate that the transcriptome of the peri-infarct region is characterized by the upregulation of genes involved in inflammation and lipid metabolism and the downregulation of genes involved in mitochondrial respiration and neuronal function. To evaluate the impact of HPβCD treatment on the transcriptome of the peri-infarct region, we also performed bulk RNA-Seq on brain tissue collected 7 weeks after DH stroke. For this analysis, we compared the peri-infarct regions of vehicle- and HPβCD-treated aged mice. The peri-infarct region of HPβCD-treated mice was characterized by 5,385 differentially expressed genes. The DE analysis revealed that peri-infarct regions of HPβCD-treated mice were characterized by the downregulation of multiple degradative enzymes, chemokine receptors, and scavenger receptors. In addition, the transcriptomic analysis demonstrated a restoration of lipid homeostasis in peri-infarct regions of HPβCD-treated mice compared to vehicle-injected mice, as evidenced by the downregulation of Lipa, Apoe, Lamp1, Npc1, and Npc2 and upregulation of Nceh1 and Ldlr. Reductions in innate and adaptive immune responses characterized peri-infarct regions of HPβCD-treated mice; these alterations are consistent with the attenuated chronic inflammation that characterized infarcts of the HPβCD-treated aged mice. These results demonstrate that HPβCD treatment after stroke attenuates chronic inflammation and promotes lipid metabolism in peri-infarct regions of aged mice. Additionally, the DE analysis revealed an upregulation of genes involved in myelin sheath structural integrity, such as Ina, Omg, and Nefl, and synaptic plasticity and neuroplasticity, such as Syn1, Bdnf, Nrg1, Negr1, and Nsg1. These results suggest that HPβCD treatment improves the structure and function of neurons in peri-infarct regions of aged mice after stroke.
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