Effect of transient focal ischemia on circular RNAs
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE115697 | GEO | 2020/09/25
REPOSITORIES: GEO
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Project description:Celastrol plays a significant role in cerebral ischemia-reperfusion injury. Although previous studies have confirmed that celastrol post-treatment has a protective effect on ischemic stroke, the therapeutic effect of celastrol on ischemic stroke and the underlying molecular mechanism remain unclear. In the present study, focal transient cerebral ischemia was induced by transient middle cerebral artery occlusion (tMCAO) in mice and celastrol was administered immediately after reperfusion. We performed lncRNA and mRNA analysis in the ischemic hemisphere of adult mice with celastrol post-treatment through RNA-Sequencing (RNA-Seq). A total of 50 differentially expressed lncRNAs (DE lncRNAs) and 696 differentially expressed mRNAs (DE mRNAs) were identified between the sham and tMCAO group, and a total of 544 DE lncRNAs and 324 DE mRNAs were identified between the tMCAO and tMCAO+celastrol group. Bioinformatic analysis was done on the identified deregulated genes through gene ontology (GO) analysis, KEGG pathway analysis and network analysis. Pathway analysis indicated that inflammation-related signaling pathways played vital roles in the treatment of ischemic stroke by celastrol. Our study suggests celastrol treatment can effectively reduce cerebral ischemia-reperfusion injury. The bioinformatics analysis of lnRNAs and mRNAs profiles in the ischemic hemisphere of adult mice provides a new perspective in the neuroprotective effects of celastrol, particularly with regards to ischemic stroke.
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Project description:Large clinical studies have shown that AT1 receptor blockers (ARBs) reduce the incidence of stroke in patients at risk. However, there is controversy about the underlying pathomechanisms. To get a closer insight into the effects of ARBs in stroke on molecular level, gene expression pattern was compared in the ischemic brain areas of Candesartan pre-treated (0,2 mg/kg bwt., 5 days, s.c.) versus vehicle treated, normotensive, adult rats after middle carotid artery occlusion (MCAO). Candesartan significantly improved neurological outcome (as estimated by Garcia-scale) 24 h and 48 h after stroke and reduced infarct volume by about 40% compared to vehicle. Experiment Overall Design: For gene expression profiling, RNA of two animals per group was pooled and forwarded to preparation of the labeled targets for the micro array experiment. For each biological condition two independent pools were hybridised onto Affymetrix RAE 230A arrays.
2008-06-12 | E-GEOD-4206 | biostudies-arrayexpress
Project description:Stroke is a leading cause of mortality and long-term disability and ischemic stroke accounts for 87% of all strokes. Though timely recanalization of the occluded vessel is essential in the treatment of ischemic stroke, it is well known to cause ischemia-reperfusion (I/R) injury which result in neuronal cell death, brain tissue loss and severe neurological deficits. In this work, we employed a global proteomic approach to examine the changes of cerebral cortex proteins in rats undergoing acute and long-term I/R injury. In vivo middle cerebral artery occlusion (MCAO) model of focal cerebral I/R injury in rats was established. The animals were divided into three model groups with 2 h-MCAO followed with different reperfusion time, 1 day, 7 days and 14 days, respectively. For each model group a sham group was correspondingly set. Each group included four animals. For proteomic analysis, cerebral cortex proteins were extracted and analyzed by SDS-PAGE, whole-lane slicing, in-gel digestion and label-free quantitative LC-MS/MS. A total of 5621 proteins were identified and their quantities between the surgery and corresponding sham groups and across the three reperfusion time points were compared for mechanism investigation. This dataset includes all the raw files of the 840 LC-MS runs (6 groups x 4 animals x 35 gel squares/sample), as well as their identification and quantitation results at the levels of peptide fragments, peptides and proteins, respectively.
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Project description:We report the application of Illumina paired-end RNA-seq approach for transcriptome of brain tissue in mice. By removing sequence-dependent bias and amplification noise using UMI-tools. The mapped reads of each sample were assembled using StringTie. After the final transcriptome was generated, StringTie and edgeR was used to estimate the expression levels of all transcripts. By obtaining a total of million paired-end reads of sequence from cerebral cortex tissue, we generated transcriptome profiles of mouse ischemic cortex in sham, 24 h after focal ischemia, 28 d after focal ischemia, with or without neuron-specific knockdown of TIPARP, respectively. We found 2017 differentially expressed genes (DEGs) between Sham+AAV-SYN-shRNA-Con and tMCAO+AAV-SYN-shRNA-Con group, and 516 DEGs between tMCAO+AAV-SYN-shRNA-Con and tMCAO+AAV-SYN-shRNA-TIPARP group at 24 h after stroke. In addition, we found 487 DEGs between Sham+AAV-SYN-shRNA-Con and tMCAO+AAV-SYN-shRNA-Con group, and 192 DEGs between tMCAO+AAV-SYN-shRNA-Con and tMCAO+AAV-SYN-shRNA-TIPARP group at 28 d after stroke. This study provides a detailed analysis of the underlying mechanisms of neuron-specific knockdown of TIPARP in neuronal injury and long-term effect, with biologic replicates, generated by RNA-seq technology.
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Project description:IL-6 Ko and wildtype control mice were subjected to 30 min left filamentous middle cerebral artery occlusion (MCAo)/reperfusion or sham operation. Animals were killed at 2 and at 10 days after MCAo or sham operation, respectively. The left (i.e. ischemic) hemisphere was used for further gene expression analysis.
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Project description:Ischemic stroke poses a significant global health burden, with rapid revascularization treatments being crucial but often insufficient to mitigate ischemia-reperfusion (I/R) injury. Dexmedetomidine (DEX) has shown promise in reducing cerebral I/R injury, but its potential molecular mechanism, particularly its interaction with non-coding RNAs (ncRNAs), remains unclear. This study investigates DEX's therapeutic effect and potential molecular mechanisms in reducing cerebral I/R injury. A transient middle cerebral artery obstruction (tMACO) model was established to simulate cerebral I/R injury in adult rats. DEX was administered pre-ischemia and post-reperfusion. RNA sequencing and bioinformatic analyses were performed on the ischemic cerebral cortex to identify differentially expressed non-coding RNAs (ncRNAs) and mRNAs. The sequencing results showed 6494 differentially expressed (DE) mRNA and 2698 DE circRNA between the sham (S) and tMCAO (I/R) groups. Additionally, 1809 DE lncRNA, 763 DE mRNA, and 2795 DE circRNA were identified between the I/R group and tMCAO+DEX (I/R+DEX) groups. Gene ontology (GO) analysis indicated significant enrichment in multicellular biogenesis, plasma membrane components, and protein binding. KEGG analysis further highlighted the potential mechanism of DEX action in reducing cerebral I/R injury, with hub genes involved in inflammatory pathways. This study demonstrates DEX's efficacy in reducing cerebral I/R injury and offers insights into its brain-protective effects, especially in ischemic stroke. Further research is warranted to fully understand DEX's neuroprotective mechanisms and its clinical applications.
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Project description:This data set shows dramatic changes in gene expression in microglia isolated from C57Bl6/J mice subjected to transient middle cerebral artery occlusion, as compared to those subjected to sham surgery. Mice deficient in Mincle (Clec4e-/-) showed significantly improved injury outcomes 3 and 7 days after transient middle cerebral artery occlusion. However, when comparing changes in gene expression in microglia 24 hours after blood reperfusion, there were no differences between wild-type and Clec4e-/- mice, indicating that Mincle does not participate in early microglial activation. Wild type and Mincle knock-out (Clec4e-/-) mice. After 1 h of transient middle cerebral artery occlusion (tMCAO) and 24 h of reperfusion, mice were perfused with PBS, their brains dissected, and 2 ipsilesional hemispheres (with cerebellum and brainstem removed) pooled for microglia isolation. For sham-operated animals, the whole forebrain was used and brains were not pooled. After myelin separation by Percoll gradient centrifugation, around 80,000 CD45intermediate, CD11b+ microglial cells were sorted from each sample. Sham samples n=3, tMCAO samples n=5.
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Project description:To investigate the effect of vascular endothelial growth factor (VEGF) on gene expression profile after focal cerebral ischemia in mouse, we employed Agilent SurePrint G3 Mouse Gene Expression 8×60K Microarray as a platform to identify which genes influenced by VEGF in mouse after focal cerebral ischemia. Mice were randomized to sham group, in which mice underwent sham surgery; MCAO group, in which transient (90 min) middle cerebral artery occlusion (MCAO) model was performed and mice received vehicle (PBS, 0.01M, pH 7.4) intracerebroventricularly in the right lateral ventricle 3hr after reperfusion; VEGF group (n = 36), in which rhVEGF-A165 (10μg/ml, dissolved in 0.01M PBS) was injected into the right lateral ventricle 3hr after reperfusion. Mice were sacrificed at 24hr after reperfusion, brains removed and peri-infarct areas were used for microarray. Gene expression microarray was applied to investigate the differentially expressed genes among sham group, MCAO group and VEGF group. Expression of thirty-seven genes was confirmed in the same RNA samples by real-time PCR.
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