Cholesterol in macrophage regulate gene expersion with or without LPS [MCD and LPS RNA-seq]
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ABSTRACT:
PROVIDER: PRJNA803746 | ENA |
REPOSITORIES: ENA
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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: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: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.
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Project description:To investigate the plasticity of Lipolysaccharide (LPS) tolerance, we employed microarray profiling to analyse the gene expression profile in macrophage. Four macrophage populations were induced; Untreated macrophages (Control group), Acute response to LPS (LPS activation group), LPS tolerance (T – Tolerant group) and recovered (R = recovered macrophage group) Using transcriptional analysis we demonstrate that recovery from LPS tolerance (R – Recovery), as defined by cytokine gene expression, is associated with a global change in the transcriptional profile of macrophage. This data confirms that LPS tolerance is a transient state which results in induction of novel hybrid macrophage activation state with a unique transcriptional signature. Bone marrow derived macrophages were polarised into three activation states; Acute response to LPS (A), LPS tolerant (T) and recovered (R). Gene expression was measured at 4 hours post stimulation with LPS. Three independent experiments were performed to measure gene expression changes between each macrophage group.
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Project description:To investigate the plasticity of Lipolysaccharide (LPS) tolerance, we employed microarray profiling to analyse the gene expression profile in macrophage. Four macrophage populations were induced; Untreated macrophages (Control group), Acute response to LPS (LPS activation group), LPS tolerance (T – Tolerant group) and recovered (R = recovered macrophage group) Using transcriptional analysis we demonstrate that recovery from LPS tolerance (R – Recovery), as defined by cytokine gene expression, is associated with a global change in the transcriptional profile of macrophage. This data confirms that LPS tolerance is a transient state which results in induction of novel hybrid macrophage activation state with a unique transcriptional signature.
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Project description:In order to fully characterize emodin's effects on macrophage activation, peritoneal macrophages were stimulated with LPS+IFNg with or without emodin and gene expression was analyzed using a whole genome microarray. Emodin significantly attenuated the IFNg/LPS induced changes in a large percentage of responsive genes (31%) through inhibiting multiple signaling pathways. RT-qPCR was used to confirm the results in several genes associated with M1 macrophage activation including: TNF, IL6, IL1b, iNOS, MMP2, and MMP9. Three-condition, one-color experiment: Vehicle control, LPS-IFNg or LPS-IFNg-Emodin treated periferal WBC PMN samples: 4 biological replicates each.
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Project description:Role of Girdin in LPS-induced macrophage polarization
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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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