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Compare RNA profile between LPS+CPN and LPS+CPN+GGOH treated peritoneal macrophages

ABSTRACT: To find out genes regulated by geranylgeraniol (GGOH) treatment in peritoneal macrophage, we compared gene expression of cells treated with 200ng ml LPS and 250 micromolar compactin versus 200ng ml LPS, 250 micromolar compactin and 100micromolar GGOH. To find out upregulated or downregulated genes regulated by GGOH treatment in peritoneal macrophage (LPS+CPN treated cell).

ORGANISM(S): Mus musculus

SUBMITTER: jinyong kim

PROVIDER: E-GEOD-48646 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Sufficient production of geranylgeraniol is required to maintain endotoxin tolerance in macrophages.

Kim Jinyong J Lee Joon No JN Ye James J Hao Rosy R Debose-Boyd Russell R Ye Jin J

Journal of lipid research 20130923 12

Endotoxin tolerance allows macrophages to produce large quantities of proinflammatory cytokines immediately after their contact with lipopolysaccharides (LPSs), but prevents their further production after repeated exposure to LPSs. While this response is known to prevent overproduction of proinflammatory cytokines, the mechanism through which endotoxin tolerance is established has not been identified. In the current study, we demonstrate that sufficient production of geranylgeraniol (GGOH) in ma ...[more]

PMID: 24062519

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Compare RNA profile between LPS+CPN and LPS+CPN+GGOH treated peritoneal macrophages

Project description:To find out genes regulated by geranylgeraniol (GGOH) treatment in peritoneal macrophage, we compared gene expression of cells treated with 200ng ml LPS and 250 micromolar compactin versus 200ng ml LPS, 250 micromolar compactin and 100micromolar GGOH.

2013-11-12 | GSE48646 | GEO

Emodin inhibits macrophage classical activation [Control-LPS-IFNg-Emodin]

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.

2016-07-04 | E-GEOD-73310 | biostudies-arrayexpress

Transcriptional profiling of macrophage plasticity following recovery from Lipopolysaccharide (LPS) tolerance

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.

2013-12-06 | E-GEOD-47783 | biostudies-arrayexpress

Mus musculus

Project description:Compare RNA profile between LPS+CPN and LPS+CPN+GGOH treated peritoneal macrophages

| PRJNA210896 | ENA

LPS induced gene expression in macrophages in the presence of Carbon monoxide

Project description:Murine RAW 264.7 peritoneal macrophages were treated with 250 ppm Carbon monoxide (CO) for 3 hours prior to the addition of LPS (10 ng/ml) and then for the subsequent 4 hours of the study. Air-treated cells were maintained for the same time without CO. Total RNA was harvested at 0, 15, 30, 60, 120 and 240 min after LPS addition. CRNA was produced using standard Affymetrix procedures from 10µg of total RNA. The expression values of all probe sets are scaled to a target intensity of 500 by using Affymetrix Microarray Suite 5.0 Keywords = macrophage Keywords = inflammation Keywords = endotoxin Keywords = gene expression Keywords: time-course

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Deep chemoproteomic analysis of LPS-stimulated RAW264.7 cell proteome

Project description:Unanticipated regulatory protein modifications can be discovered from the unbiased comprehensive analysis of biological systems using SAMPEI. To explore this idea, we sought to map protein modifications induced during mammalian cell differentiation, modeled by the response of mouse RAW264.7 macrophage cells to lipopolysaccharide (LPS), a potent inducer of macrophage activation and differentiation that involves extensive protein and metabolic signaling.

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miRNA profiling in mouse peritoneal macrophages treated without or with LPS

Project description:We have identified a number of miRNAs that are differentially expressed in LPS treated mouse peritoneal macrophages, as compared to untreated cells Peritoneal macrophages treated with LPS for 0, 4, 12, 24h. RNA was isolated and miRNA array assays were performed by Exiqon (miRCURY™ LNA Array version 10.0)

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LPS upregulates palmitoylated enzymes of the phosphatidylinositol cycle. An insight from proteomic studies.

Project description:The studies aim at revealing changes of the level of fatty-acylated proteins induced by LPS in RAW264 macrophage-like cells

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RNA sequencing of corticospinal neurons and control callosal projection neurons purified from the cerebral cortex of adult wild-type and Sod1G86R mice, a model of amyotrophic lateral sclerosis, at four disease-relevant ages.

Project description:Amyotrophic Lateral Sclerosis is clinically defined as the combined degeneration of the corticospinal and corticobulbar neurons (CSN) along with the bulbar and spinal motor neurons (SMN). While a growing body of evidence points to the motor cortex, where CSN are located, as the potential initiation site of ALS, little is known about how CSN degenerate. To gain insights into the molecular mechanisms behind CSN selective degeneration, we first developed an approach to purify this neuronal population from the cerebral cortex of adult wild-type and Sod1G86R mice, combining retrograde labelling and Fluorescence Activated Cell Sorting. In parallel, a second population of cortical neurons, the callosal projection neurons (CPN) located in the layers II/III of the cerebral cortex were also purified. CPN and CSN are both cortical excitatory projection neurons but as opposed to CSN, CPN do not degenerate in Sod1G86R mice, and served as control population. CSN and CPN were purified from same animals, at two presymptomatic ages (3 and 60 days) and two symptomatic ages, 90 and 105 days. A total of 57 samples were further processed and analysed (CSN: 30d: n=4 WT and 3 Sod1G86R; 60d: n=4 WT and 4 Sod1G86R; 90d: n=4 WT and 4 Sod1G86R; 105d: n=4 WT and 2 Sod1G86R; CPN: 30d: n=4 WT and 3 Sod1G86R; 60d: n=2 WT and 3 Sod1G86R; 90d: n=4 WT and 4 Sod1G86R; 105d: n=4 WT and 4 Sod1G86R).

2020-12-30 | E-MTAB-7876 | biostudies-arrayexpress

Real-time quantitative PCR analysis of ARF-deficient macrophages

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2011-09-29 | E-GEOD-32446 | biostudies-arrayexpress

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