Ontology highlight
ABSTRACT:
PROVIDER: PRJNA809756 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18116800_1.fastq.gz | Fastqsanger.gz | |||
| SRR18116800_2.fastq.gz | Fastqsanger.gz | |||
| SRR18116801_1.fastq.gz | Fastqsanger.gz | |||
| SRR18116801_2.fastq.gz | Fastqsanger.gz | |||
| SRR18116802_1.fastq.gz | Fastqsanger.gz |
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Project description:RNA-Seq transcriptome comparison of the following cell populations (n=4 independent samples per cell population): a) CD11c-eYFP+ cells FACS sorted from brain of adult mice 4 days after cerebral ischemia, b) CX3CR1+ microglia sorted from the ischemic brain of CX3CR1CreERT2-ROSA26 tdTomato mice; c) CD11c-rYFP+ cells sorted from the spleen of control mice; d) CX3CR1+ microglia sorted from the brain of control mice. Purpose: The goal of this study is to compare the transcriptome profile (RNA-Seq) of cD11c-eYFP+ cells and microglia, both collected from ischemic brains of mice, and with reference cell populations, i.e. Steady-stated microglia from brain of corresponding control mice and steady-state CD11c-eYFP cells sorted from the spleen of control mice. Methods: RNA samples were obtained from FACS sorted eYFP+ cells of the ipsilateral brain hemisphere of CD11c-eYFP mice 4 days post-ischemia, the spleen of control CD11c-eYFP mice, and from microglial cells sorted from control brain and the ipsilateral brain hemisphere 4 days post-ischemia of Cx3cr1CreERT2:ROSA26dTomato mice. NGS was perfomed (RNA-Seq) to compare the transcriptome of these populations. Results: the populations we compared clearly separated the differentially expressed genes in an unsupervised cluster analysis. 950 genes were overrepresented in microglia and 1469 genes were overrepresented in CD11c-eYFP+ cells in the ischemic brain. Conclusions: Our study is the first comparative analysis of the transcriptomes of microglia and the infiltrating CD11c-eYFP+ cells derived from the ischemic brain of mice. The results show that the infiltrating CD11c-eYFP cell population in the ischemic brain tissue of parabiotic mice displays overrepresentation of genes typical of dendritic cells, immune functions, and ClassII antigen presentation, amongst others, that are not found represented in microglia.
2020-10-20 | GSE136852 | GEO
Project description:RNA-Seq transcriptome comparison of the following cell populations (n=3-4 independent samples per cell population): a) CD11c-eYFP+ cells FACS sorted from brain of female adult mice 4 days after cerebral ischemia, b) CD11c-eYFP+ cells FACS sorted from brain of female parabiotic mice 4 days after cerebral ischemia c) CX3CR1+ microglia sorted from the ischemic brain of female CX3CR1CreERT2-ROSA26 tdTomato mice. Purpose: The goal of this study is to compare the transcriptome profile (RNA-Seq) of infiltrating cD11c-eYFP+ cells and microglia, both collected from ischemic brains of mice. Methods: RNA samples were obtained from FACS sorted eYFP+ cells of the ipsilateral brain hemisphere of CD11c-eYFP mice 4 days post-ischemia, the ipsilateral brain hemisphere of CD11c-eYFP/WT parabiotic mice 4 days post-ischemia, and from microglial cells sorted from the ipsilateral brain hemisphere of Cx3cr1CreERT2:ROSA26dTomato mice 4 days post-ischemia. NGS was performed (RNA-Seq) to compare the transcriptome of these populations. Results: the populations we compared clearly separated the differentially expressed genes in an unsupervised cluster analysis. 1509 genes were overrepresented in microglia and 1183 genes were overrepresented in CD11c-eYFP+ cells in the ischemic brain. Conclusions: Our study is the first comparative analysis of the transcriptomes of microglia and the infiltrating CD11c-eYFP+ cells derived from the ischemic brain of mice. The results show that the infiltrating CD11c-eYFP cell population in the ischemic brain tissue of parabiotic mice displays overrepresentation of genes typical of dendritic cells, immune functions, and ClassII antigen presentation, amongst others, that are not found represented in microglia.
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Project description:Microglia are resident CNS immune cells that are active sensors in healthy brain and versatile effectors under pathological conditions. Cerebral ischemia induces a robust neuroinflammatory response that includes marked changes in the gene expression and phenotypic profile of a variety of endogenous CNS cell types (astrocytes, neurons, microglia) as well as an influx of leukocytic cells (neutrophils, macrophages, T-cells) from the periphery. Many molecules and conditions can trigger a transformation of ârestingâ (or surveying) microglia to an âactivatedâ (alerted/reactive) state. Here we review recent developments in the literature that relate to microglial activation in the experimental setting of in vitro and in vivo ischemia. We also present new data from our own laboratory demonstrating the direct effects of in vitro ischemic conditions on the microglial phenotype and genomic profile. Emphasis is placed on the role of specific molecular signaling systems such as hypoxia inducible factor-1 (HIF-1) and toll-like receptor-4 (TLR4) in regulating the microglial response in this setting. We then review histological and recent novel radiological data that confirms a key role for microglial activation in the setting of ischemic stroke in humans. We discuss recent progress in the pharmacological and molecular targeting of microglia in acute ischemic stroke. Finally, we explore how recent studies on ischemic preconditioning have increased interest in preemptively targeting microglial activation in order to reduce stroke severity. 12 arrays, 4 experimental groups, 3 replicates in each group, CN is control normoxia, CH is control hypoxia, TN is TLR4 knockout normoxia, TH is TLR4 knockout hypoxia.
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Project description:PGC-1α overexpression in microglia protects against ischemia-induced brain damage in mice. To investigate the underlying mechanism of PGC-1α, we have employed whole mRNA microarray expression profiling as a discovery platform to identify genes with the potential to change the microglial function. Indeed, PGC-1α overexpression alters the gene expression profiles of microglia after AIS, this suggested that microglial PGC-1α might play an important role after ischemic stroke.
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