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Macrophage miR-210 induction and metabolic reprogramming in response to pathogen interaction boost life-threatening inflammation.

ABSTRACT: RNAseq was performed on murine bone marrow-derived macrophages (BMDMs) untreated and following 42 hours LPS/IFN-g treatment.

ORGANISM(S): Mus musculus

PROVIDER: GSE171270 | GEO | 2021/04/01

REPOSITORIES: GEO

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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

Macrophage miR-210 induction and metabolic reprogramming in response to pathogen interaction boost life-threatening inflammation.

Project description:Macrophage miR-210 induction and metabolic reprogramming in response to pathogen interaction boost life-threatening inflammation.

| PRJNA718874 | ENA

ChIP-seq to profile LPS-induced RNA polymerase II transcription in bone marrow-derived macrophages from WT and Hes1 KO mice

Project description:We characterized the RNA polymerase II occupancy on gene loci in WT and Hes1 KO BMDMs under untreated and LPS-stimulated conditions WT and Hes1 KO BMDMs were left untreated or stimulated with LPS for 1 hour. Pol II ChIP was performed and the DNA products were subject to ChIPseq

2016-06-13 | E-GEOD-73568 | biostudies-arrayexpress

Kinetics of LPS induction in wt and Cop1-ko BMDMs

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2018-10-03 | GSE114762 | GEO

ChIPseq to profile CDK9 and Hes1 occupancy in bone marrow-derived macrophages from C57BL/6 mice

Project description:We characterized the CDK9 and Hes1 occupancy on gene loci in conditions of unstimuated and LPS stimualtion in BMDMs BMDMs were left untreated or stimulated with LPS for 1 hour. CDK9 or Hes1 ChIP was performed and the DNA products were subject to ChIPseq

2016-06-13 | E-GEOD-77334 | biostudies-arrayexpress

ChIP-seq to profile LPS-induced RNA polymerase II transcription in bone marrow-derived macrophages from WT and Hes1 KO mice

Project description:We characterized the RNA polymerase II occupancy on gene loci in WT and Hes1 KO BMDMs under untreated and LPS-stimulated conditions

2016-06-13 | GSE73568 | GEO

GPR35 mediates lysophosphatidic acid-signaling in bone marrow-derived macrophages at the transcriptional level

Project description:Purpose: Our previous experiments showed that LPA activated inhibitory G-protein signaling in human GPR35-transfected cells. We wanted to test the LPA signaling in presence or absence of GPR35. Methods: We isolated RNA from bone-marrow derived macrophages (BMDMs) from WT or GPR35-deficient mice that were treated with LPA or LPS, and left untreated for control. Results: We have found that GPR35-deficiency alters the transcriptional profiles in response to LPA in BMDMs. On the other hand, LPS-treated WT and GPR35-deficient BMDMs showed similar transcriptional changes. Conclusion: GPR35-deficientcy alters the LPA but not LPS signaling.

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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

STAT3 regulates pathogen control and clearance in macrophages by reprogramming inflammation-induced microbial defense response

Project description:STAT3 is pivotal in controlling hyperinflammation and governing effector macrophage responses to inflammation, yet the precise mechanisms by which STAT3 mediates pathogen control and clearance remain unclear. Herein, we performed RNA sequencing in bone marrow derived macrophages (BMDMs) to investigate STAT3-mediated transcriptional regulation of LPS-induced inflammation. Genome-wide profiling revealed significant enrichment of type-I interferon (IFN-I) associated genes and the IFN Gamma response pathway in Stat3-deficient BMDMs in homeostasis. We observed significant reduction in the expression of pathogen response genes and secretion of cytokines and chemokines associated with pathogen clearance in Stat3-deficient BMDMs upon LPS stimulation. Using BM chimeric mice with 20% Stat3-deficient hematopoietic cells infected with Citrobacter rodentium, we show that STAT3 is essential for preventing bacterial dissemination to tissues and regulating production of cytokines and chemokines related to immune cell recruitment and bacterial control. Stat3-deficient BMDMs infected with C. rodentium showed impaired ability to kill intracellular bacteria and demonstrated dampened expression of pathogen response genes. Further, IL-6 blockade subdued the intrinsic IFN signature in Stat3-deficient macrophages and rescued aberrant expression of pathogen response genes upon LPS stimulation, suggesting STAT3 restrains an aberrant autocrine IL-6 signal that deregulates macrophage-mediated pathogen control. Our data identifies novel functions for STAT3 in orchestrating an optimal microbial defense response, by promoting bacterial control and clearance in macrophages.

2025-11-22 | GSE282695 | 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

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