Isolated astrocytes from young BMAL1aKO and wildtype mice
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ABSTRACT:
PROVIDER: PRJNA945943 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR23901643_1.fastq.gz | Fastqsanger.gz | |||
| SRR23901643_2.fastq.gz | Fastqsanger.gz | |||
| SRR23901645_1.fastq.gz | Fastqsanger.gz | |||
| SRR23901645_2.fastq.gz | Fastqsanger.gz |
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Project description:Purpose: The core clock protein BMAL1 serves as the primary positive circadian transcriptional regulator and its depletion in astrocytes not only disrupts circadian function, but also leads to a unique cell-autonomous activation phenotype. We have undertaken RNAsequencing of isolated astrocytes from young wildtype and BMAL1 astrocyte-specific knockout mice (Bmal1fl/fl, ALDH1L1-CreERT2, termed BMAL1 aKO) to uncover changes to gene expression as a result of BMAL1 disruption in astrocytes. Methods: BMAL1 aKO mice and wildtype littermates were given tamoxifen at 2 months of age and harvested around 7 months of age and brains were collected. After collagenase digestion and debris removal, astrocytes were isolated from the rest of the brain cells (termed "flowthrough") using Miltenyi MACS Anti-ACSA-2 magnetic beads. RNA was extracted in Trizol reagent and sent for sequencing. Samples from BMAL1 aKO and wildtype astrocytes were compared and flowthrough samples were compared to astrocytes to confirm cell-type purity. Results: BMAL1 aKO results in both up- and down-regulation of many astrocyte genes. GO pathway analysis points to lysosomal pathways as dysregulated by knockout of BMAL1 in astrocytes. While astrocytes are enriched by our isolation methods, there is some degree of contamination from neurons and oligodendrocytes. Conclusions: While our astrocyte isolation method has some caveats in terms of purity, BMAL1 aKO appears to dysregulate lysosomal pathways, which will be investigated by further experiments.
2023-04-26 | GSE227633 | GEO
Project description:Isolated astrocytes from aged BMAL1aKO and wildtype mice
| PRJNA947531 | ENA
Project description:Purpose: The core clock protein BMAL1 serves as the primary positive circadian transcriptional regulator and its depletion in astrocytes not only disrupts circadian function, but also leads to a unique cell-autonomous activation phenotype. We have undertaken RNAsequencing of isolated astrocytes from aged wildtype and BMAL1 astrocyte-specific knockout mice (Bmal1fl/fl, ALDH1L1-CreERT2, termed BMAL1 aKO) to uncover changes to gene expression as a result of BMAL1 disruption in astrocytes and to confirm those changes persist during aging. Methods: BMAL1 aKO mice and wildtype littermates were given tamoxifen at 2 months of age and harvested around 20 months of age and brains were collected. After collagenase digestion and debris removal, astrocytes were isolated from the rest of the brain cells (termed "flowthrough") using Miltenyi MACS Anti-ACSA-2 magnetic beads. RNA was extracted in Trizol reagent and sent for sequencing. Samples from BMAL1 aKO and wildtype astrocytes were compared and flowthrough samples were compared to astrocytes to confirm cell-type purity. Results: BMAL1 aKO results in both up- and down-regulation of many astrocyte genes. GO pathway analysis points to lysosomal pathways as dysregulated by knockout of BMAL1 in astrocytes. While astrocytes are enriched by our isolation methods, there is some degree of contamination from neurons and oligodendrocytes. Conclusions: While our astrocyte isolation method has some caveats in terms of purity, BMAL1 aKO appears to dysregulate lysosomal pathways, which will be investigated by further experiments.
2023-04-26 | GSE227932 | GEO
Project description:RNA-seq of astrocytes isolated from parental isolated mice
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Project description:Isolation of glia from Alzheimer's mice reveals inflammation and dysfunction. Reactive astrocytes and microglia are associated with amyloid plaques in Alzheimer's disease (AD). Yet, not much is known about the molecular alterations underlying this reactive phenotype. To get an insight into the molecular changes underlying AD induced astrocyte and microglia reactivity, we performed a transcriptional analysis on acutely isolated astrocytes and microglia from the cortex of aged controls and APPswe/PS1dE9 AD mice. As expected, both cell types acquired a proinflammatory phenotype, which confirms the validity of our approach. Interestingly, we observed that the immune alteration in astrocytes was relatively more pronounced than in microglia. Concurrently, our data reveal that astrocytes display a reduced expression of neuronal support genes and genes involved in neuronal communication. The microglia showed a reduced expression of phagocytosis and/or endocytosis genes. Co-expression analysis of a human AD expression data set and the astrocyte and microglia data sets revealed that the inflammatory changes in astrocytes were remarkably comparable in mouse and human AD, whereas the microglia changes showed less similarity. Based on these findings we argue that chronically proinflammatory astrocyte and microglia phenotypes, showing a reduction of genes involved in neuronal support and neuronal signaling, are likely to contribute to the neuronal dysfunction and cognitive decline in AD. 2 cell types from 2 conditions: cortical microglia and cortical astrocytes from 15-18 month old APPswe/PS1dE9 mice compared to wildtype littermates. Biological replicates: microglia from APPswe/PS1dE9, N=7, microglia from WT, N=7, astrocytes from APPswe/PS1dE9, N=4, microglia from WT, N=4
2015-11-04 | E-GEOD-74615 | biostudies-arrayexpress
Project description:Reactive astrogliosis is characterized by a profound change in astrocyte phenotype in response to all CNS injuries and diseases. To better understand the reactive astrocyte state, we used Affymetrix GeneChip arrays to profile gene expression in populations of reactive astrocytes isolated at various time points after induction using two different mouse injury models, ischemic stroke and neuroinflammation. Young adult male mice underwent middle cerebral artery occlusion (MCAO) to produce ischemic stroke or control sham surgery. Young adult mice were injected intraperitoneally with 5 mg/kg lipopolysaccharide (LPS) to produce neuroinflammation or saline for control. Astrocytes were acutely purified from control and injured brains at 1 day after injury for LPS/saline injection and 1, 3 days and 7 days after MCAO/sham surgeries.
2012-05-01 | E-GEOD-35338 | biostudies-arrayexpress
Project description:GFAP and vimentin deficiency alters gene expression in astrocytes and microglia in wild-type mice and changes the transcriptional response of reactive glia in mouse model for Alzheimer's disease. Reactive astrocytes with an increased expression of intermediate filament (IF) proteins Glial Fibrillary Acidic Protein (GFAP) and Vimentin (VIM) surround amyloid plaques in Alzheimer's disease (AD). The functional consequences of this upregulation are unclear. To identify molecular pathways coupled to IF regulation in reactive astrocytes, and to study the interaction with microglia, we examined WT and APPswe/PS1dE9 (AD) mice lacking either GFAP, or both VIM and GFAP, and determined the transcriptome of cortical astrocytes and microglia from 15- to 18-month-old mice. Genes involved in lysosomal degradation (including several cathepsins) and in inflammatory response (including Cxcl5, Tlr6, Tnf, Il1b) exhibited a higher AD-induced increase when GFAP, or VIM and GFAP, were absent. The expression of Aqp4 and Gja1 displayed the same pattern. The downregulation of neuronal support genes in astrocytes from AD mice was absent in GFAP/VIM null mice. In contrast, the absence of IFs did not affect the transcriptional alterations induced by AD in microglia, nor was the cortical plaque load altered. Visualizing astrocyte morphology in GFAP-eGFP mice showed no clear structural differences in GFAP/VIM null mice, but did show diminished interaction of astrocyte processes with plaques. Microglial proliferation increased similarly in all AD groups. In conclusion, absence of GFAP, or both GFAP and VIM, alters AD-induced changes in gene expression profile of astrocytes, showing a compensation of the decrease of neuronal support genes and a trend for a slightly higher inflammatory expression profile. However, this has no consequences for the development of plaque load, microglial proliferation, or microglial activation. 2 cell types from 6 conditions: cortical microglia and cortical astrocytes from 15-18 month old APPswe/PS1dE9 mice compared to wildtype littermates. Biological replicates: microglia from APPswe/PS1dE9, N=7, microglia from WT, N=7, astrocytes from APPswe/PS1dE9, N=4, microglia from WT, N=4
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Project description:Isolation of glia from Alzheimer's mice reveals inflammation and dysfunction. Reactive astrocytes and microglia are associated with amyloid plaques in Alzheimer's disease (AD). Yet, not much is known about the molecular alterations underlying this reactive phenotype. To get an insight into the molecular changes underlying AD induced astrocyte and microglia reactivity, we performed a transcriptional analysis on acutely isolated astrocytes and microglia from the cortex of aged controls and APPswe/PS1dE9 AD mice. As expected, both cell types acquired a proinflammatory phenotype, which confirms the validity of our approach. Interestingly, we observed that the immune alteration in astrocytes was relatively more pronounced than in microglia. Concurrently, our data reveal that astrocytes display a reduced expression of neuronal support genes and genes involved in neuronal communication. The microglia showed a reduced expression of phagocytosis and/or endocytosis genes. Co-expression analysis of a human AD expression data set and the astrocyte and microglia data sets revealed that the inflammatory changes in astrocytes were remarkably comparable in mouse and human AD, whereas the microglia changes showed less similarity. Based on these findings we argue that chronically proinflammatory astrocyte and microglia phenotypes, showing a reduction of genes involved in neuronal support and neuronal signaling, are likely to contribute to the neuronal dysfunction and cognitive decline in AD.
2015-11-04 | GSE74615 | GEO
Project description:We analyzed the transcriptional profile of astrocytes from 1) WT mice infected with AAV-GFP, 2) reactive astrocytes from 9-month old APP/PSdE9 mice infected with AAV-GFP and 3) de-activated astrocytes from 9-month old APP/PSdE9 mice infected with AAV-SOCS3 We show SOCS3 normalizes the inflammatory profile of APP astrocytes
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Project description:We report RNA-seq of single myofibers with different p21 expression level isolated from EDL muscle of young and old mice.
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