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Gene expression differences between LPS, anti-CD36 Abs, or LPS plus anti-CD36 Abs treated RAW264.7 cells.

ABSTRACT: Gene expression differences between LPS, anti-CD36 Abs, or LPS plus anti-CD36 Abs treated RAW264.7 cells.

PROVIDER: PRJNA1226949 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32454964_1.fastq.gz	Fastqsanger.gz
	SRR32454964_2.fastq.gz	Fastqsanger.gz
	SRR32454965_1.fastq.gz	Fastqsanger.gz
	SRR32454965_2.fastq.gz	Fastqsanger.gz
	SRR32454966_1.fastq.gz	Fastqsanger.gz

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Gene expression differences between LPS, anti-CD36 Abs, or LPS plus anti-CD36 Abs treated RAW264.7 cells.

Project description:To comprehensively analyze the transcriptome of macrophages treated with LPS, anti-CD36 Abs, or LPS plus anti-CD36 Abs, respectively, we employed RNA sequencing (RNA-seq) assay

2025-02-24 | GSE290268 | GEO

Oxidized Lipids and CD36-Mediated Lipid Peroxidation in CD8 T Cells Suppress Anti-Tumor Immune Responses

Project description:T cell metabolic fitness plays a pivotal role in anti-tumor immunity and metabolic deregulation causes T cell dysfunction in cancer. We identify that CD36 limits anti-tumor CD8+ T cell effector functions through lipid peroxidation. In murine tumors, oxidized phospholipids (OxPLs) were highly abundant and CD8+ TILs increased uptake and accumulation of lipids and lipid peroxidation. Functionally ‘exhausted’ CD8+ TILs increased CD36 expression and CD36-deficient CD8+ TILs had more robust anti-tumor activity and cytokine production than wild-type cells. We further show that CD36 promotes uptake of oxidized low-density lipoproteins (OxLDL), induces lipid peroxidation in CD8+ TILs, and enhances p38 kinase phosphorylation. Moreover, we found that OxLDL inhibits CD8+ T cell functions in a CD36/p38-dependent manner. Furthermore, glutathione peroxidase 4 (GPX4) over-expression lowers lipid peroxidation and restores functionalities in CD8+ TILs. These results define a key role for an oxidized lipid-CD36-p38 axis in promoting intratumoral CD8+ T cell dysfunction.

2021-03-31 | GSE171194 | GEO

CD36 deficiency causes intestinal extracellular matrix disruption and chronic neutrophil

Project description:BACKGROUND & AIMS: The scavenger receptor CD36 has versatile immuno-metabolic actions. CD36 is abundantly expressed in the small intestinal epithelium but its impact on gut homeostasis is unknown. METHODS: Wild type (WT) and CD36-null (CD36KO) mice were fed a chow diet and small intestinal morphology assessed by immunohistochemistry and electron microscopy (EM). Inflammation was evaluated from neutrophil infiltration, expression of cytokines and toll-like receptors. Barrier integrity was determined using FITC-dextran and circulating lipopolysaccharide (LPS). Enterocyte (Ent-CD36KO) and endothelial (EC-CD36KO) CD36 null mice were generated to test contribution of epithelial versus endothelial CD36 to the intestinal phenotype. RESULTS: The small intestine of CD36KO mice fed a chow diet showed abnormal remodeling of the extracellular matrix (ECM) with altered expression of ECM and junction proteins. Hypertrophy of cell junctions and basement membranes was observed by EM. The CD36KO intestines displayed neutrophil infiltration, inflammation and compromised barrier function. Systemic leukocytosis and neutrophilia were present in CD36KO mice and there was 80% reduction of anti-inflammatory Ly6Clow monocytes important for ECM regulation and tissue repair. Bone marrow transplants supported primary contribution of tissue injury in initiation of inflammation. Studies with Ent-CD36KO mice did not support a major contribution of enterocyte CD36 while endothelial CD36 deficiency associated with neutrophil infiltration, aberrant expression of tight junctions and inflammation in the small intestine. CONCLUSION: CD36 is important for maintenance of barrier function in the small intestine. CD36 deletion causes ECM remodeling with collagen accumulation, depletion of the Ly6Clow monocyte subset and chronic inflammation. Endothelial but not enterocyte CD36 loss is a significant contributor to the spontaneous inflammation.

2016-10-01 | GSE73569 | GEO

PLT012, a humanized CD36-blocking antibody, is effective for unleashing anti-tumor immunity against liver cancer and liver metastasis

Project description:Tumor cells develop various strategies to evade immune surveillance, one of which is the modulation of the metabolic state of the tumor microenvironment (TME). In response to metabolic stress in the TME, several tumor-infiltrating immune subsets upregulate CD36 to take up lipids. This leads to impaired anti-tumor immunity, as intratumoral regulatory T cells (Tregs) exhibit increased survival and suppressive activity, while CD8+ T cells become more susceptible to ferroptosis and exhaustion. Here, we develop a humanized anti-CD36 IgG4 antibody, PLT012, against the lipid-binding domain of CD36 with excellent safety and favorable pharmacokinetic features in mice and cynomolgus monkey. PLT012 alone or in combination with PD-L1 blockade or standard-of-care immunotherapy results in robust anti-tumor immunity in both immunotherapy-sensitive and -resistant hepatocellular carcinomas (HCCs). Notably, PLT012 also reprograms immune landscape of human HCC ex vivo. Our findings provide proof-of-concept evidence that PLT012 effectively reprograms anti-tumor immunity in HCC, positioning it as a first-in-class immunotherapy targeting CD36.

2025-04-11 | GSE291964 | GEO

Transcription profiling of mouse IL-10 -/- macrophages treated with LPS/LPS plus IL10 reveals a transcriptional repressor and co-repressor induced by the STAT3-regulated anti-inflammatory signaling pathway.

Project description:IL-10 regulates anti-inflammatory signaling via the activation of STAT3, which in turn controls the induction of a gene expression program whose products execute inhibitory effects on pro-inflammatory mediator production. Here we show that IL-10 induces the expression of an ETS family transcriptional repressor, ETV3 and a helicase family co-repressor, SBNO2 (Strawberry notch homolog 2) in mouse and human macrophages. IL-10-mediated induction of ETV3 and SBNO2 expression was dependent upon both STAT3, and co-stimulus through the TLR pathway. We also observed that ETV3 expression was strongly induced by the STAT3 pathway induced by IL-10 but not STAT3 signaling activated by IL-6, which cannot activate the anti-inflammatory signaling pathway. ETV3 and SBNO2 specifically repressed NF-kB-mediated transcription and can physically interact. Collectively our data suggest that ETV3 and SBNO2 are components of the pathways that contribute to the downstream anti-inflammatory effects of IL-10. We compared expression profiles of macrophages isolated from IL-10 -/- mice. Macrophages were treated with either LPS or LPS plus IL-10. Treatment times were 10, 20 and 30 minutes. Experiment Overall Design: Mouse IL-10 -/- macrophages were isolated and purified and set up in culture medium containing LPS or LPS plus IL-10. A total of 18 samples were analyzed. This set contains three replicates of each treatment condition where treatment (LPS versus LPS plus IL-10) and time (10min, 20min and 30min) were varied.

2008-06-16 | E-GEOD-9509 | biostudies-arrayexpress

AMSC CD36+ subpopulations

Project description:AMSC CD36+ subpopulations

| PRJNA783325 | ENA

Gene expression of RAW 264.7 cells treated with LPS, ISO, PGE2, LPS PLUS ISO, and LPS PLUS PGE2

Project description:LPS plus ISO and LPS plus PGE2 had non-additive effects on gene expression in RAW 264.7 cells Keywords: time course

2006-06-06 | GSE4964 | GEO

Gene expression of RAW 264.7 cells treated with LPS, IFG, 2MA, LPS PLUS IFG, and LPS PLUS 2MA

Project description:LPS plus IFG and LPS plus 2MA had non-additive effects on gene expression in RAW 264.7 cells Keywords: time course

2006-06-06 | GSE4962 | GEO

Anti-inflammatory role of low intensity pulsed ultrasound in inhibiting LPS-induced M1 polarization of RAW264.7 via Wnt2b/AXIN/β-catenin

Project description:Low-intensity pulsed ultrasound (LIPUS) is a special type of low intensity ultrasound. In periodontal disease, LIPUS was applied as an adjuvant and non-invasive therapeutic treatment. While, the specific mechanism of LIPUS in the treatment of periodontal disease is not quite clear.RAW264.7 cells were induced to M1/M2 macrophage-like polarization by LPS/IL4. LIPUS was performed to stimulate RAW264.7 cells at an intensity of 45 mW/cm2, 25 min, interval 24 h, twice. The polyA mRNA sequencing of LPS induced RAW264.7 cells, LPS induced and LIPUS treated RAW264.7 cells were conducted.Our results suggested that LIPUS played an anti-inflammatory role by inhibiting LPS-induced M1 polarization of RAW264.7 cells in an Wnt2b/AXIN/β-catenin dependent way. LIPUS may inhibit inflammation in periodontal diseases by regulating macrophage differentiation, so as to play a therapeutic role in periodontal diseases.

2024-10-15 | GSE273466 | GEO

AMSC CD36+ subpopulations

Project description:Adipose-derived MSCs (AMSC) are currently utilized in clinical trials for various diseases including osteoarthritis, amyotrophic lateral sclerosis, and multiple system atrophy. Whilst AMSCs may be defined by the surface expression of classical markers including CD44, CD90, CD105, and absence of CD45, these cells may exhbit donor-to-donor differences in differentiation potential. In this study we evaluated the expression of CD36 amongst AMSCs and utilized magnetic cell sorting to enrich for CD36+ cells. Whole transcriptome RNA-sequencing was performed on unsorted, CD36+ enriched, and CD36+ depleted cells to determine gene expression difference between these populations of cells. CD36 sorted or unsorted cells were then plated and maintained in growth medium. Cells were expanded for 2 passages and passage 8 cells were plated for RNA-sequencing analysis. Trizol reagent was used to harvest cells when they were proliferating cells (~80%) or 100% confluent cells.

2021-11-28 | GSE189525 | GEO

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