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Disease-associated astrocyte epigenetic memory promotes CNS pathology [RNA-Seq of p300 KD, ACLY KD and scramble NOD-EAE mice]

ABSTRACT: Disease-associated astrocyte epigenetic memory promotes CNS pathology [RNA-Seq of p300 KD, ACLY KD and scramble NOD-EAE mice]

PROVIDER: PRJNA1060769 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27411754_1.fastq.gz	Fastqsanger.gz
	SRR27411754_2.fastq.gz	Fastqsanger.gz
	SRR27411755_1.fastq.gz	Fastqsanger.gz
	SRR27411755_2.fastq.gz	Fastqsanger.gz
	SRR27411756_1.fastq.gz	Fastqsanger.gz

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Disease-associated astrocyte epigenetic memory promotes CNS pathology [RNA-Seq of p300 KD, ACLY KD and scramble NOD-EAE mice]

Project description:Gene profiling of scramble, ACLY, and p300 KD astrocytes during NOD-EAE in B6 mice.

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Genome-wide analysis of the transcriptional profile of sphingolipid-related genes KD astrocytes during EAE in NOD mice.

Project description:We reported that knockdown of sphingolipid metabolism in astrocytes has impact to interfere EAE pathological progressing in NOD mice

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Analysis of a non-obese diabetes-experimental autoimmune encephalomyelitis (NOD-EAE)

Project description:The purpose of this study was to analyze and elucidate the mechanisms of non-obese diabetes-experimental autoimmune encephalomyelitis (NOD-EAE), an animal model of progressive multiple sclerosis (MS), and to compare the pathological features with those observed in human progressive MS. To achieve this, pathological analysis, flow cytometry analysis, immunohistochemical staining, and transcriptome analysis were performed at each pathological stage of the NOD-EAE mice to characterize each pathological stages in the lesion. In the chronic phase of the NOD-EAE mice, fibrosis and lymph follicle formation, characteristic of progressive human MS, were observed. We describe the pathological profile and transcriptome analysis of the NOD-EAE mice and verify that this model has similar features to those of human progressive MS. Our findings suggest that this model recapitulates lymph follicle formation, a disease hallmark of progressive MS, and fibrosis, a feature complicating the pathogenesis of MS in the chronic phase.

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Pharmacologic or genetic inhibition of EphB3 receptor kinase impacts CNS pathology during progressive EAE

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Genome-wide analysis of the transcriptional profile of sphingolipid-related genes KD astrocytes during EAE in NOD mice.

Project description:Genome-wide analysis of the transcriptional profile of sphingolipid-related genes KD astrocytes during EAE in NOD mice.

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ACLY and ACC1 Regulate Hypoxia-Induced Apoptosis by Modulating ETV4 via Î±-ketoglutarate

Project description:In order to propagate a solid tumor, cancer cells must adapt to and survive under various tumor microenvironment (TME) stresses, such as hypoxia or lactic acidosis. To systematically identify genes that modulate cancer cell survival under stresses, we performed genome-wide shRNA screens under hypoxia or lactic acidosis. We discovered that genetic depletion of acetyl-CoA carboxylase (ACACA or ACC1) or ATP citrate lyase (ACLY) protected cancer cells from hypoxia-induced apoptosis. Additionally, loss of ACLY or ACC1 reduced levels and activities of the oncogenic transcription factor ETV4. Silencing ETV4 also protected cells from hypoxia-induced apoptosis and led to remarkably similar transcriptional responses as with silenced ACLY or ACC1, including an anti-apoptotic program. Metabolomic analysis found that while Î±-ketoglutarate levels decrease under hypoxia in control cells, Î±-ketoglutarate is paradoxically increased by hypoxia when ACC1 or ACLY are depleted. Supplementation with Î±-ketoglutarate rescued the hypoxia-induced apoptosis and recapitulated the decreased expression and activity of ETV4 via an epigenetic mechanism. Therefore, ACC1 and ACLY regulate the levels of ETV4 under hypoxia via increased Î±-ketoglutarate. These results reveal that ACC1/ACLY- Î±-ketoglutarate-ETV4 is a novel means by which metabolic states regulate transcriptional output for life vs. death decisions under hypoxia. Since many lipogenic inhibitors are under investigation as cancer therapeutics, our findings suggest that the use of these inhibitors will need to be carefully considered with respect to oncogenic drivers, tumor hypoxia, progression and dormancy. More broadly, our screen provides a framework for studying additional tumor cell stress-adaption mechanisms in the future. DESIGN: H1975 lung cancer cells transduced with a scramble shRNA hairpin or two different shRNAs against ACLY, ACC1, or ETV4 under hypoxia.

2015-12-10 | E-GEOD-61286 | biostudies-arrayexpress

Expression data by ACLY knockdown

Project description:De novo lipogenesis is activated in most cancers. Several lipogenic enzymes are implicated in oncogenesis and represent potential cancer therapeutic targets. RNA interference-mediated depletion of ATP citrate lyase (ACLY), the enzyme that catalyzes the first step of de novo lipogenesis, leads to growth suppression in a subset of human cancer cells. Here we demonstrate the molecular basis and potential biomarkers for ACLY-targeting therapy. First, suppression of cancer cell growth by ACLY depletion involves down-regulation of fatty acid elongase ELOVL6 at the transcriptional level. Lipid profiling revealed that ACLY depletion alters fatty acid composition in triglyceride; increased palmitate and decreased longer fatty acids, in accordance with ELOVL6 down-regulation. Second, ACLY depletion increases reactive oxygen species (ROS), whereas addition of antioxidant reduces ROS and attenuates the growth suppression. Third, ACLY depletion or ROS stimulation induce phosphorylation of AMP-activated protein kinase (AMPK), a sensor of energy and lipid metabolism. Analysis of various cancer cell lines revealed that the levels of AMPK phosphorylation (p-AMPK) correlate with the basal ROS levels, and that cancer cells with low basal p-AMPK (i.e., low basal ROS) levels are highly susceptible to ACLY depletion-mediated growth suppression. Finally, in clinical colon cancer tissues, p-AMPK levels are significantly decreased in aggressive tumors and correlate with the levels of 8-hydroxydeoxyguanosine, a hallmark of ROS stimulation. Together, these data suggest that ACLY inhibition suppresses cancer growth via palmitate-mediated lipotoxicity, and p-AMPK could be a predictive biomarker for its therapeutic outcome. Two cell lines are treated with ACLY siRNA. The samples include controls of each cell line.

2014-04-13 | E-GEOD-37243 | biostudies-arrayexpress

Analysis of a non-obese diabetes-experimental autoimmune encephalomyelitis (NOD-EAE)

Project description:Analysis of a non-obese diabetes-experimental autoimmune encephalomyelitis (NOD-EAE)

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CD4+ T cells have different gene profiles between Ogt-KD and control mice after EAE

Project description:To investigate whether the level of O-GlcNAc could affect CD4+ T cell function after EAE, we performed RNA-sequencing analysis on splenic CD4+ T cells. The downregulation of OGT in CD4+ T cells led to changes in gene expression profile in CD4+ T cells with a 2-fold threshold. Next, Gene Ontology (GO) analysis was performed to compare differentially expressed genes in Ogt-KD and control mice. These results indicated that OGT was involved in the regulation of multiple important cellular events.

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Expression data by ACLY knockdown

2014-04-13 | GSE37243 | GEO