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Gene expression signatures before or after transient middle cerebral artery oclussion (tMCAO) in ZEB1 transgenic and wild type mice

ABSTRACT: Gene expression signatures before or after transient middle cerebral artery oclussion (tMCAO) in ZEB1 transgenic and wild type mice

PROVIDER: PRJNA432941 | ENA |

REPOSITORIES: ENA

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Gene expression signatures before or after transient middle cerebral artery oclussion (tMCAO) in ZEB1 transgenic and wild type mice

Project description:To further development of the role of ZEB1 in microglia, we have employed whole mRNA microarray expression profiling as a discovery platform to identify genes. Mouse microglia from wild type(wt), ZEB1-overexpression(ZEB1-tg) and ZEB1 knock down(ZEB1-kd) mice were isolated before and after tMCAO. The result showed after tMCAO, the wild type, ZEB1-overexpression and ZEB1 knock down microglia displayed a different gene profile, this suggested microglia ZEB1 might play an important role after ischemic stroke.

2018-03-07 | GSE110141 | GEO

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Effect of Celastrol on LncRNAs and mRNAs Profiles of Cerebral Ischemia-Reperfusion Injury in Transient Middle Cerebral Artery Occlusion Mice Model

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: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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Effect of dexmedetomidine on ncRNA and mRNA profiles of cerebral ischemia-reperfusion injury in transient middle cerebral artery occlusion rats model

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Rattus norvegicus brain tissue samples: Sham-operated vs. Remote limb postconditioning (PostC) and Sham-operated vs. transient middle cerebral artery occlusion (tMCAO)

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Rattus norvegicus brain tissue samples: Sham-operated vs. Remote limb postconditioning (PostC) and Sham-operated vs. transient middle cerebral artery occlusion (tMCAO)

Project description:Rattus norvegicus brain tissue samples: Sham-operated vs. Remote limb postconditioning (PostC) and Sham-operated vs. transient middle cerebral artery occlusion (tMCAO)

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The role of a mammalian network in regulating ischemic stroke outcome II

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Single-cell analyses reveal the dynamic functions of Itgb2+ microglia subclusters at different stages of cerebral ischemia-reperfusion injury in transient middle cerebral occlusion mice model

Project description:The underlying pathophysiological mechanisms of cerebral ischemia-reperfusion injury (CIRI) is intricate, and current studies suggest that neuron, astrocyte, microglia, endothelial cell, and pericyte all have different phenotypic changes of specific cell types after ischemic stroke. And microglia account for the largest proportion after CIRI. Previous transcriptomic studies of ischemic stroke have typically focused on the 24 hours after CIRI, obscuring the dynamics of cellular subclusters throughout the disease process. Therefore, traditional methods for identifying cell types and their subclusters may not be sufficient to fully unveil the complexity of single-cell transcriptional profile dynamics caused by an ischemic stroke. In this study, to explore the dynamic transcriptional profile of single cells after CIRI, we used scSTAR, a new bioinformatics method, to analyze the single cell transcriptional profile of day 1, 3 and 7 of transient middle cerebral artery occlusion (tMCAO) mice. Combining our bulk RNA sequence and proteomics data, we found that the Itgb2+ subclusters of microglia exhibited specific functions at three different time points after the tMCAO. Our further analysis revealed that the Itgb2+ microglia subcluster was mainly involved in energy metabolism, cell cycle, angiogenesis, neuronal myelin formation and repair at 1, 3 and 7 days after tMCAO, respectively. Our results suggested that Itgb2+ microglia act as a time-specific multifunctional immunomodulatory subcluster during CIRI, and the underlying mechanisms remain to be further investigated.

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