Cholesterol in macrophage regulate gene expersion with or without LPS [MCD and LPS RNA-seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA803746 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17893402_1.fastq.gz | Fastqsanger.gz | |||
| SRR17893402_2.fastq.gz | Fastqsanger.gz | |||
| SRR17893403_1.fastq.gz | Fastqsanger.gz | |||
| SRR17893403_2.fastq.gz | Fastqsanger.gz | |||
| SRR17893404_1.fastq.gz | Fastqsanger.gz |
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Project description:cholesterol reduction in macrophages by methyl-b-cyclodextran (MCD) or statin alters gene expression. When activated by inflammatory stimilus LPS, macrophages responded in a cholesterol specific fashion.
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Project description:cholesterol reduction in macrophages by methyl-b-cyclodextran (MCD) or statin alters gene expression. When activated by inflammatory stimilus LPS, macrophages responded in a cholesterol specific fashion.
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Project description:Cholesterol in macrophage regulate gene expersion with or without LPS [statin and LPS RNA-seq]
| PRJNA803745 | ENA
Project description:We performed comparative studies of monocytes trained by either PBS, cholesterol or varying dosages of LPS, in order to examine the differential innate responses to stress signals. Differentially trained monocytes were subjected to whole genome methylation array analyses. Our data reveal that monocytes trained by either cholesterol or very low dose LPS preferentially clustered together in terms of their genome methylation profiles, separate from the naïve PBS treated monocytes or monocytes trained by high dose LPS. Our findings suggest that monocytes may similarly respond to the generic membrane stress signals caused by either very low dose LPS or cholesterol, in contrast to the exhausted state induced by high dose LPS.
2024-09-10 | GSE243358 | GEO
Project description:The mitogen-activated protein kinase (MAPK) p38 pathway is reported to regulate macrophage responses to lipopolysaccharide (LPS) at least partly via the phosphorylation of the mRNA-destabilizing factor tristetraprolin (TTP). LPS-activated MAPK p38 phosphorylates and activates the downstream kinase MAPK-activated protein kinase 2 (MK2), which then phosphorylates serines 52 and 178 of TTP, resulting in loss of mRNA-destabilizing activity. As a consequence, mRNAs that contain binding sites for TTP are stabilized in a manner that is acutely sensitive to the activity of the MAPK p38 pathway. Dual specificity phosphatase 1 (DUSP1) dephosphorylates and inactivates MAPK p38. Dusp1-/- macrophages overexpress a number of pro-inflammatory mediators, but their genome-wide responses to LPS have not yet been described in detail. Dusp1-/- mice are exceptionally sensitive to a wide variety of inflammatory challenges, including experimental models of endotoxemia or sepsis. It has been suggested (but not yet proven) that DUSP1 controls the inflammatory response of macrophages in part via the regulation of MAPK p38 activity and TTP phosphorylation status. We generated a mouse knock-in strain, in which codons 52 and 178 of the endogenous Zfp36 gene (which encodes TTP) were mutated to alanine codons. The mutation gives rise to a constitutively active form of TTP, which cannot be inactivated via the p38 MAPK pathway. The Zfp36aa/aa strain was back-crossed against C57/BL6 for > 10 generations. We also generated a double-targeted strain in which the Zfp36 mutation was combined with disruption of the Dusp1 gene. This expression array describes LPS responses of primary mouse bone marrow-derived macrophages of four genotypes, and closely matched genetic background: wild type (Dusp1+/+ : Zfp36+/+); TTP mutant (Zfp36aa/aa); DUSP1 knock out (Dusp1-/-); and double targeted (Dusp1-/- : Zfp36aa/aa). The data provide a comprehensive picture of the impact of Dusp1 deletion or TTP mutation on the responses of primary macrophages to LPS. They also demonstrate that the excessive inflammatory responses of Dusp1-/- macrophages are largely a consequence of the phosphorylation and inactivation of TTP. Genome wide expression profiles of wild type, Dusp1-/-, Zfp36aa/aa and Dusp1-/-/Zfp36aa/aa M-CSF derived macrophages, stimulated with LPS for 1 or 4 hours
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Project description:We fed control mice and Slc7a11-LTG mice methionine and Choline Deficient (MCD) to induce NASH. Whole-genome RNA sequencing were then performed in the livers of control and LTG mice fed with MCD.
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Project description:Introduction: Minimal change disease (MCD) is a major cause of nephrotic syndrome. With a substantial number of patients requiring long-term immunosuppression leading to significant morbidity, the study aim was to determine MCD glomerular transcriptome to serve as a basis for biomarker discovery and novel drug target identification. Animal work showed podocyte injury induced by IL-7/IL-7R signaling (Zhai S, BBRC, 2018). Methods: Renal biopsies from adult patients representing the following groups were selected from the Norwegian Kidney Biopsy Registry: MCD (n=14), as well as normal tissue (n=8) and primary membranous nephropathy (MN; n=12) as the two reference groups. RNA for 75 base-pair paired-end RNASeq was obtained by dissecting glomeruli via laser capture microdissection (LCM) from FFPE cross-sections. Systematic delineation of condition-specific alteration in transcriptional landscapes was achieved by combining pathway-centered analyses with methodologies derived from network science and integrating multiple bioinformatics resources. Results: Compared to normal glomeruli, glomeuli from MCD displayed an inflammatory signature that appeared to be predominantly governed by the IL1 and IL7 systems. While enrichment of IL1 production and secretion was a shared feature of MCD and MN compared to normal tissue, responses involving IL7 pathway activation were unique to MCD. Indeed, IL7R expressed by glomeruli was the most up-regulated gene of to the interleukin-family in MCD vs normal controls. IL7 pathway activation was paralleled by significant enrichment in adaptive immune system processes and transcriptional regulation and depletion in pathways related to energy metabolism and transcription. Downregulation of these organ function-related themes again occurred predominately in MDC and were significantly less pronounced in MN. Conclusion: Our results demonstrate that archival FFPE-biopsies can be used to generate glomeruli-specific gene expression profiles suitable for systematic delineation of kidney-associated diseases. Here the latter provides a data-driven rationale to experimentally address these MCD-specific features as biomarkers and as novel drug targets. In this context inhibiting activation of the IL7 pathway may be particularly promising.
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Project description:The microRNAs expression was markedly altered with the MCD diet. Using a custom microarray platform, we analyzed the expression levels of 1135 mouse microRNA probes in liver tissue that were fed MCD diet.
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Project description:Healing of the cutaneous wound requires macrophage recruitment at the sites of injury, where chemotactic migration of macrophages toward the wound is regulated by local inflammation. Recent studies suggest a positive contribution of DNA methyltransferase 1 (Dnmt1) to macrophage pro-informatory responses; however, its role in regulating macrophage motility remains unknown. In this study, myeloid-specific depletion of Dnmt1 in mice promoted cutaneous wound healing and de-suppressed the lipopolysaccharides (LPS)-inhibited macrophage motility. Dnmt1 inhibition in macrophages eliminated the LPS-stimulated changes in cellular mechanical properties in terms of elasticity and viscoelasticity. LPS increased the cellular accumulation of cholesterol in a Dnmt1-depedent manner; cholesterol content determined cellular stiffness and motility. Lipidomic analysis indicated that Dnmt1 inhibition altered the cellular lipid homeostasis, probably through down-regulating the expression of cluster of differentiation 36 CD36 (facilitating lipid influx) and up-regulating the expression of ATP-binding cassette transporter ABCA1 (mediating lipid efflux) and sterol O-acyltransferase 1 SOAT1 (also named ACAT1, catalyzing the esterification of cholesterol). Our study revealed a Dnmt1-dependent epigenetic mechanism in the control of macrophage mechanical properties and the related chemotactic motility, indicating Dnmt1 as both a marker of diseases and a potential target of therapeutic intervention for wound healing.
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Project description:Genome wide DNA methylation profiling of human normal and epileptic brain tissue. The Illumina Infinium 850K Human DNA methylation Beadchip was used to obtain DNA methylation profiles across approximately 850.000 CpGs in formalin-fixed paraffin-embedded surgical brain samples. Samples included 316 cases diagnosed with malformations of cortical development (MCD), non-MCD epilepsy or no-epilepsy autopsy controls.
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