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MiRNA array for LPS-activated tnc+/+ and tnc-/- macrophages

ABSTRACT: Endogenous molecules generated upon pathogen invasion or tissue damage serve as danger signals that activate host defence, however their precise immunological role remains unclear. Tenascin-C is an extracellular matrix glycoprotein that is specifically induced upon injury and infection. We have shown that its expression is required to generate an effective immune response to bacterial lipopolysaccharide (LPS) during experimental sepsis in vivo. Tenascin-C enables macrophage translation of pro-inflammatory cytokines upon LPS activation of toll-like receptor 4 (TLR4) and suppresses the synthesis of anti-inflammatory cytokines. It mediates post-transcriptional control of a specific subset of inflammatory mediators via induction of the microRNA miR-155. Thus tenascin-C plays a key role in regulating the inflammatory axis during pathogenic activation of TLR signaling. The data deposited here include the analysis of miRNA profile of tnc+/+ and tnc-/- bone marrow-derived macrophages (BMDMs) following stimulation with LPS for 8 hours.

ORGANISM(S): Mus musculus Rattus norvegicus

PROVIDER: GSE41584 | GEO | 2012/10/18

SECONDARY ACCESSION(S): PRJNA177589

REPOSITORIES: GEO

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miRNA array for LPS-activated tnc+/+ and tnc-/- macrophages

Project description:Endogenous molecules generated upon pathogen invasion or tissue damage serve as danger signals that activate host defence, however their precise immunological role remains unclear. Tenascin-C is an extracellular matrix glycoprotein that is specifically induced upon injury and infection. We have shown that its expression is required to generate an effective immune response to bacterial lipopolysaccharide (LPS) during experimental sepsis in vivo. Tenascin-C enables macrophage translation of pro-inflammatory cytokines upon LPS activation of toll-like receptor 4 (TLR4) and suppresses the synthesis of anti-inflammatory cytokines. It mediates post-transcriptional control of a specific subset of inflammatory mediators via induction of the microRNA miR-155. Thus tenascin-C plays a key role in regulating the inflammatory axis during pathogenic activation of TLR signaling. The data deposited here include the analysis of miRNA profile of tnc+/+ and tnc-/- bone marrow-derived macrophages (BMDMs) following stimulation with LPS for 8 hours. Bone marrow-derived macrophages (BMDMs) were cultured in complete DMEM medium, non-stimulated or stimulated for 8 hours with 100ng/ml LPS and total RNA was extracted. Samples were analysed with TaqMan Low Density Arrays (Applied Biosystems).

2012-10-18 | E-GEOD-41584 | biostudies-arrayexpress

Effects of tenascin-C on gene expression in mouse mammary gland tumor

Project description:Tenascin-C (TNC), a cancer-associated extracellular matrix glycoprotein, plays a pivotal role in tumor growth. However, the mechanism whereby TNC affects tumor biology remains unclear. We used microarrays to investigate change in global gene expression between tumors in wild-type (WT) mice, which express TNC, and tumors in TNC-knockout (TNKO) mice. We developed a non-TNC-producing mouse mammary tumor cell line (GLMT1). GLMT1 was inoculated in the drosal flank of WT mice and TNKO mice. After 14 days, the tumor were harvested and RNA was extracted. Subsequently, they were processed and hybridized on Affymetrix GeneChip Mouse Genome 430 2.0 Array

2016-02-10 | E-GEOD-77739 | biostudies-arrayexpress

Genome-wide RNA sequencing analysis in Il10-/- bone marrow-derived macrophages stimulated by lipopolysaccharide

Project description:We report the genome-wide RNA sequencing analysis in Il10-/- bone marrow-derived macrophages (BMDMs) stimulated by lipopolysaccharide (LPS) where IL-10 effect in macrophage inflammatory response was examined in IL-10-deficient BMDMs upon LPS stimulation with addition of exogenous IL-10.

2018-11-02 | GSE122070 | GEO

Genomic features enabling control of inflammatory gene expression by antagonistic signals

Project description:BMDMs or iMACs were generated via differentiation of bone marrow cells or immortalized precursors, respectively, in culture media containing m-CSF for 7 day. Upon differentiation, BMDMs or iMacs were left untreated or stimulated as described below. 1) BMDM WT were stimulated with LPS, PGE2, IL-10, LPS+PGE2, LPS+IL-10 for 4 hours: each condition in triplicate. This experiment was performed to assess chromatin accessibility in the concomitant presence of pro-inflammatory (LPS) and anti-inflammatory stimuli (PGE2 and IL-10). 2) MEF2A-deficient iMac clones (D7, A7, A8, C7) and MEF2A-proficient (referred to as wild-type) iMac clones (NE, B3 and D10) were generated via CRISPR/Cas9 and stimulated or not with LPS for either 4 hours: each condition in single. This experiment was performed to assess the role in MEF2a in controlling chromatin accessibility upon LPS stimulation.

2021-06-08 | E-MTAB-9252 | biostudies-arrayexpress

Gene expression profiles of inoculated tumor cells in TNC-KO mice

Project description:Tenascin-C (TNC), a cancer-associated extracellular matrix glycoprotein, plays a pivotal role in tumor growth. To identify the genes regulated by TNC during tumor growth, we performed a tumor growth assay, DNA microarray analysis, and quantitative real-time PCR (qRT-PCR). Mouse mammary tumor cells were subcutaneously inoculated into GRS/A (WT) and GRS/A-TgH(Tnc) (TNKO) mice. Tumors in WT mice significantly increased in volume with expressing TNC while tumors in TNKO mice showed hardly detectable levels of TNC. Tumor gene expression profiles between TNKO and WT mice were compared using DNA microarray analysis. We found that 447 genes were up-regulated (TNKO>WT) and 667 genes were down-regulated (TNKO<WT) in the TNKO group. We then classified these genes by Gene Ontology (GO) terms in order to elucidate their biological function. There were three GO terms found related to tumor growth, namely, “acute inflammatory response”, “cell adhesion”, and “response to wounding”. Eighty-three of the genes primarily involved in these GO terms were further validated by qRT-PCR. Eight genes: Tnc, Cxcl2, Cxcl1, Hbegf, Chl1, Cd44, Serpina3n, and F3 were significantly down-regulated relative to the WT. Eighteen genes: Saa3, P2rx7, Ptgs1, Ptger2, Comp, Steap4, Il1rn, Il1b, Ncf1, Mst1, Nfκb1, Ctsb, Tnfrsf1a, Tnfrsf1b, Cd24a, Adam17, Mtpn, and Sox4 were significantly up-regulated relative to the WT. These results support our hypothesis that TNC has multi-faceted effects on both the tumor cells and their microenvironment. First, TNC acts on the tumor cells directly by up-regulating genes involved in cancer cell proliferation through the CXCL1/2 and CXCR2 pathway. Second, TNC controls the tumor microenvironment by promoting angiogenesis through the CXCL1/2 and CXCR2 pathway, and by suppressing inflammatory gene expression through a separate pathway.

2017-09-07 | GSE67896 | GEO

Lactic acid modifies gene expression and chromatin accessibility of bone marrow-derived macrophages during lipopolysaccharide stimulation (RNA-seq and ATAC-seq)

Project description:Lactic acid (LA) has emerged as an important modulator of immune cell function. We performed ATAC-seq to profile the chromatin landscape of bone marrow-derived macrophages (BMDMs) upon lipopolysaccharide (LPS) stimulation with or without LA. Additionally, we also report the genome-wide RNA sequencing analysis in bone marrow-derived macrophages (BMDMs) where LA effect in macrophage inflammatory response was examined in BMDMs upon lipopolysaccharide (LPS) stimulation in the presence or absence of LA. To further examine LA effect due to low pH, hydrochloric acid (HCl) was used to adjust similar pH conditions (i.e. pH 6.5) as in media with LA.

2024-01-16 | GSE253050 | GEO

CTRP6 promotes macrophage inflammatory response and its deficiency attenuates LPS-induced inflammation

Project description:Macrophages play critical roles in inflammation and tissue homeostasis, and their functions are regulated by various autocrine, paracrine, and endocrine factors. We have previously shown that CTRP6, a secreted protein of the C1q family, targets both adipocytes and macrophages to promote obesity-linked inflammation in adipose tissue. However, the gene programs and signaling pathways directly regulated by CTRP6 in macrophage remain unknown. Here, we combine transcriptomic and phosphoproteomic analyses to show that CTRP6 activates inflammatory gene programs and signaling pathways in bone marrow-derived macrophages (BMDMs). Treatment of BMDMs with CTRP6 upregulates proinflammatory, and suppresses the anti-inflammatory, gene expression. We show that CTRP6 activates p44/42-MAPK, p38-MAPK, and NF-κB signalings to promote inflammatory cytokine secretion from BMDMs, and that pharmacologic inhibition of these signaling pathways largely abolish the effects of CTRP6. Pretreatment of BMDMs with CTRP6 further augments LPS-induced inflammatory signaling and cytokine secretion from BMDMs. Consistent with the metabolic phenotype of proinflammatory M1-like macrophages, CTRP6 treatment induces a shift toward aerobic glycolysis and lactate production, reduces oxidative metabolism, and elevates mitochondrial ROS production in BMDMs. We use a Ctrp6 knockout mouse model to further confirm the physiologic relevance of our in vitro findings. BMDMs from CTRP6-deficient mice are less inflammatory at baseline and show a marked suppression of LPS-induced inflammatory gene expression and cytokine secretion. Loss of CTRP6 in mice also dampens LPS-induced inflammation and hypothermia. Collectively, we provide mechanistic evidence that CTRP6 regulates macrophage function, and neutralizing CTRP6 activity may have beneficial effects in reducing inflammation.

2024-01-26 | PXD042268 | Pride

Comparison of tenascin-C proficient versus tenascin-C deficient Mouse Embryonic Fibroblasts (MEFs)

Project description:In order to investigate what signalling pathways are turned on by tenascin-C, we generated Mouse Embryonic Fibroblasts (MEFs) deficient for tenascin-C and compared their gene expression profile to MEFs proficient for tenascin-C. TNC-KO MEFs as well as WT MEFs in which tenascin-C was knocked-down (following stable transfection of a short hairpin RNA) were compared to WT MEFs (expressing strong endogenous levels of tenascin-C).

2011-02-22 | E-GEOD-23547 | biostudies-arrayexpress

Effect of tenascin C on brain tumor initiating cells

Project description:We have determined that tenascin C (TNC) regulates the growth of human brain tumor initiating cells (BTICs). We have identified novel mechanisms by which TNC regulates BTIC growth. Analysis of the array data identified a number of genes that were altered with TNC treatment that could potentially regulate BTIC growth. The study provides the mechanistic basis for the regulation of BTIC growth with TNC.

2017-02-08 | GSE94640 | GEO

Induction of type I interferons in macrophages requires MEF2A and is targeted by prostaglandin E2

Project description:BMDMs were generated via differentiation of bone marrow cells in culture media containing m-CSF for 7 day. Upon differentiation, BMDMs were left untreated or stimulated with LPS, IFNa, PGE2, LPS+PGE2, or IFNa+PGE2.

2021-06-01 | E-MTAB-9253 | biostudies-arrayexpress

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