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Resolving monocytes generated through TRAM deletion attenuate the pathogenesis of atherosclerosis

ABSTRACT: We performed scRNAseq analysis of murine monocytes cultured from bone marrow isolates of WT and TRAM knockout mice. WT and TRAM knockout monocytes were cultured in vitro for 5 days in the presence or absence of low dose LPS (100 pg/ml).

ORGANISM(S): Mus musculus

PROVIDER: GSE182237 | GEO | 2021/11/10

REPOSITORIES: GEO

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Resolving monocytes generated through TRAM deletion attenuate the pathogenesis of atherosclerosis

Project description:Resolving monocytes generated through TRAM deletion attenuate the pathogenesis of atherosclerosis

| PRJNA755439 | ENA

Generation of resolving neutrophils with 4-PBA or genetic deletion of TRAM

Project description:We have generated resolving neutrophils with anti-inflammatory potency, through applying the pharmacological agent 4-PBA or genetically depleting TRAM molecule. WT murine neutrophils treated with PBS or 4-PBA for overnight were harvested for scRNAseq analysis to examine the generated resolving neutrophil phenotype. In addtion, we have cultured WT and TRAM KO neutrophils and compared the resolving phenotype via scRNAseq analysis.

2022-04-20 | GSE182356 | GEO

Resolving monocytes generated through TRAM deletion attenuate atherosclerosis.

Project description:Polarization of low-grade inflammatory monocytes facilitates the pathogenesis of atherosclerosis. However, underlying mechanisms as well as approaches for resolving monocyte polarization conducive to the regression of atherosclerosis are not well established. In this report, we demonstrate that TRIF-related adaptor molecule (TRAM) mediated monocyte polarization in vivo and in vitro. TRAM controlled monocyte polarization through activating Src family kinase c-SRC, which not only induces STAT1/STAT5-regulated inflammatory mediators CCR2 and SIRP-α but also suppresses PPARγ-regulated resolving mediator CD200R. Enhanced PPARγ and Pex5 due to TRAM deficiency facilitated peroxisome homeostasis and reduction of cellular reactive oxygen species, further contributing to the establishment of a resolving monocyte phenotype. TRAM-deficient monocytes propagated the resolving phenotype to neighboring monocytes through CD200R-mediated intercellular communication. At the translational level, we show that TRAM-deficient mice were resistant to high-fat diet-induced pathogenesis of atherosclerosis. We further document that intravenous transfusion of TRAM-deficient resolving monocytes into atherosclerotic mice potently reduced the progression of atherosclerosis. Together, our data reveal that targeting TRAM may facilitate the effective generation of resolving monocytes conducive for the treatment of atherosclerosis.

| S-EPMC8564896 | biostudies-literature

Monocyte exhaustion mediated by TRAM

Project description:We performed single cell sequencing analysis of exhausted monocytes generated in vitro through prolonged incubation with high dose LPS. We demonstated that 5-day prolonged stimulation of WT but not TRAM KO monocytes with high dose LPS drastically induced monocyte exhaustion, as reflected in higher levels of inflammatory marker genes such as CD38 and immuno-suppressor genes including PD-L1.

2021-10-22 | GSE182355 | GEO

Human PDA Cell Lines: single cell RNA-Sequencing after treatment with Trametinib (TRAM) and/or Hydroxychloroquine (HCQ)

Project description:Several Human PDA Cell Lines (ASPC1, PANC1, KP4, HPAFII, PATU8988S, PK45H, S2013, CAPAN1, BXPC3, HPAC, SW1990, MIAPACA2) were cultured and treated with DMSO, Trametinib (TRAM), Hydroxychloroquine (HCQ) and the combination of them before being prepared for Single-Cell RNA Sequencing

2026-01-16 | GSE310584 | GEO

Monocyte exhaustion mediated by TRAM

Project description:Monocyte exhaustion mediated by TRAM

| PRJNA755992 | ENA

Generation of resolving neutrophils with 4-PBA or genetic deletion of TRAM

Project description:Generation of resolving neutrophils with 4-PBA or genetic deletion of TRAM

| PRJNA755993 | ENA

M-TraM analysis for identification of chlorhexidine resistance genes in Enterococcus faecium E1162

Project description:Microarray-based Transposon Mapping (M-TraM) of E. faecium E1162 to identify conditionally essential genes, required for growth in the presence of chlorhexidine (1.2 ug/ml)

2016-07-03 | E-MTAB-4173 | biostudies-arrayexpress

Resolving neutrophils due to TRAM deletion renders protection against experimental sepsis.

Project description:ObjectiveProper inflammation resolution is crucial to prevent runaway inflammation during sepsis and reduce sepsis-related mortality/morbidity. Previous studies suggest that deleting TRAM, a key TLR4 signaling adaptor, can reprogram the first inflammatory responder cell-neutrophil from an inflammatory state to a resolving state. In this study, we aim to examine the therapeutic potential of TRAM-deficient neutrophils in vivo with recipient mice undergoing experimental sepsis.Material and methodsWild-type or Tram-/- mice were intraperitoneally injected with cecal slurry to induce either severe or mild sepsis. Phenotypic examinations of sepsis and neutrophil characteristics were examined in vivo and ex vivo. The propagations of resolution from donor neutrophils to recipient cells such as monocytes, T cells, and endothelial cells were examined through co-culture assays in vitro. The efficacies of Tram-/- neutrophils in reducing inflammation were studied by transfusing either wild-type or Tram-/- neutrophils into septic recipient mice.ResultsTram-/- septic mice had improved survival and attenuated injuries within the lung and kidney tissues as compared to wild-type septic mice. Wild-type septic mice transfused with Tram-/- resolving neutrophils exhibited reduced multi-organ damages and improved cellular homeostasis. In vitro co-culture studies revealed that donor Tram-/- neutrophils can effectively propagate cellular homeostasis to co-cultured neighboring monocytes, neutrophils, T cells as well as endothelial cells.ConclusionsNeutrophils with TRAM deletion render effective reprogramming into a resolving state beneficial for ameliorating experimental sepsis, with therapeutic potential in propagating cellular and tissue homeostasis as well as treating sepsis.

| S-EPMC10727485 | biostudies-literature

Bulk RNAseq of BMDM-T cells co-culture system with or without tumor antigen and IL-1beta or IL-18

Project description:To investigate the transcriptome changes of BMDM-T cell co-culture system, spleen lyphocytes were cultured with WT or Tmem175-/- BMDMs in 1640 supplied with FBS, m-CSF, and IL-2 for 48 hours. Tumor antigens, IL-1beta (500 pg/ml), or IL-18 (500 pg/ml) were added during the co-culture period. At the end of the culture, cells were harvested for RNA seq.

2026-01-19 | GSE291434 | GEO

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