Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single cell RNA sequencing of peritoneal cells from macrophage-Cd36-/- and macrophage-Cd36 fl/fl mice at the resolution phase of sterile inflammation.

ABSTRACT: Single cell RNA sequencing of peritoneal cells from macrophage-Cd36-/- and macrophage-Cd36 fl/fl mice at the resolution phase of sterile inflammation.

PROVIDER: PRJNA867562 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Single cell RNA sequencing of peritoneal cells from macrophage-Cd36-/- and macrophage-Cd36 fl/fl mice at the resolution phase of sterile inflammation.

Project description:Monocytes and macrophages as components of innate immunity are critical for both homeostasis and inflammation. The scavenger receptor CD36, highly expressed in macrophages, promotes immunological responses mediated by recognition of molecular patterns on pathogens or endogenous ligands on apoptotic cells. CD36 mediated lipid uptake also allows metabolic adaptations that influence macrophage phenotype and polarization. CD36 binds diverse lipids including fatty acids and various lipoproteins, which could exert differential effects on macrophage conversion. Previous studies reported opposite outcomes due to CD36-mediated lipid uptake; macrophages converted to either an inflammatory or an alternatively activated phenotype. To determine the role of this receptor in vivo in the presence of physiological lipid sources, we created macrophage-specific CD36 knockout mice. Using zymosan-induced peritonitis to activate immune cells, we show through single cell RNA sequencing analysis that a broad variety of resident and infiltrated immune cells are present in the peritoneum 72h after the initial stimulus. CD36 deficiency did not affect the numbers of cells during the infiltration and resolution phases, but CD36 deficiency altered the macrophage transcriptome. Pathways related to innate immunity, antigen presentation and oxidative phosphorylation were upregulated in macrophages with CD36 deficiency, whereas those related to efferocytosis, adaptive immunity and B cell activation were downregulated. Despite these gene changes, neither immunoglobulin production nor peritoneal efferocytosis was altered by macrophage CD36 deficiency, nor were there changes in the numbers of circulating white blood cells. Thus, CD36 deficiency does not reduce the inflammatory phenotype of induced peritoneal macrophages.

2024-05-31 | GSE210795 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and cd36-/- murine peritoneal macrophage Transcriptomes

Project description:Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and cd36-/- murine peritoneal macrophage Transcriptomes

| PRJNA579834 | ENA

Bone marrow derived macrophage vs peritoneal macrophage

Project description:Bone marrow derived macrophage vs peritoneal macrophage

| PRJNA414129 | ENA

Transcriptomic analysis of peritoneal macrophages from MED1 fl/fl and macrophage MED1 KO mice

Project description:Purpose: The goal of this study is to obtain the differential gene expression in MED1fl/fl and MED1ΔMac peritoneal macrophages (PMs) stimulated with or without LPS. Methods: Pooled PMs were collected from 8-week-old MED1fl/fl and MED1ΔMac mice (n=6 mice/group), and then treated without or with lipopolysaccharide (LPS; 50 ng/mL) for 6 hours. PMs mRNA profiles were generated by deep sequencing, in duplicate, using Illumina NextSeq500. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: reads were mapped to the mm9 whole genome using tophat and RPKM were calculated using cufflink. qRT–PCR validation was performed using SYBR Green assays. Results: Using an optimized data analysis workflow, we mapped about 12 million sequence reads per sample to the mouse genome (build mm9) and identified 24,130 transcripts in the PMs of MED1fl/fl and MED1ΔMac mice. Data analysis with TopHat and Cufflinks workflows revealed a significant overlap yet provided complementary insights in transcriptome profiling. Conclusions: Our study represents the detailed analysis of PMs transcriptomes, with biologic replicates, generated by RNA-seq technology. Our results show that the expression of more than 20 genes involved in innate immune response and M1 polarization was significantly higher in MED1ΔMac than in MED1fl/fl macrophages after LPS treatment. Upregulated genes in MED1ΔMac macrophages are the proinflammatory genes.

2022-02-17 | GSE196680 | GEO

Precision N-glycoproteomics of murine peritoneal macrophage

Project description:In this study, we profiled the precision N-glycoproteome of the murine peritoneal macrophage under different stimulation.

2021-06-12 | PXD026629 | Pride

Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and cd36-/- murine peritoneal macrophage Transcriptomes

Project description:Oxidized LDL induce macrophages to turn into foam cells in a CD36 dependent manner. The Goal of this study is to compare transcriptome profile by RNA-seq among WT/CD36 knockout macrophages treated with or without oxLDL. We detected re-organization of lipid metabolisms as well as immune activation by oxLDL.

2019-10-28 | GSE139439 | GEO

Peritoneal macrophage heterogeneity in decompensated liver cirrhosis

Project description:Peritoneal macrophage heterogeneity in decompensated liver cirrhosis

| PRJNA514059 | ENA

Bone marrow derived macrophage vs peritoneal macrophage

Project description:Immunometabolism is a rapidly growing field, which has led to greater understanding of innate immune cell functions. Macrophages are at the core of this research: polarized subsets of in vitro-derived cells reportedly utilize select metabolic pathways to maintain their phenotype. However, relevance of these in vitro studies to the in vivo setting is not known, and metabolic requirements are likely dependent on unique physiological and cellular metabolic environments. Here we define the metabolic requirements of peritoneal tissue-resident macrophages, the accessibility of these metabolites to cells in the peritoneum, and we dissect the role of this unique environment in maintaining a crucial macrophage function. We find that the peritoneal cavity is enriched in amino acids, most notably glutamate. Peritoneal tissue-resident macrophages have an extraordinarily large mitochondrial capacity compared with other phagocytes; this is primarily fueled by glutaminolysis, which is additionally required to maintain an extensive respiratory burst. Glutaminolysis fuels the electron transport chain, which is enhanced during tissue-resident macrophage respiratory burst via a switch to dependence of mitochondrial complex-II. This is not dependent on the level of NADPH, but requires p47 maintained NADPH-oxidase activity. Therefore, we propose that tissue-resident macrophages exploit their unique metabolic niche by implementing their glutamine-fueled mitochondrial-rich phenotype to sustain respiratory burst to assault pathogens, showing that cell-specific metabolic underpinning is important for function. Importantly, we also find that glutamine is required for the respiratory burst in human monocytes, which highlights that metabolites are not species-specific and can be the link between cellular mechanism in mouse and man.

2017-10-13 | GSE104920 | GEO

Astragaloside IV attenuates macrophage-derived exosomes induced peritoneal fibrosis after inflammatory injury through the miR-204-5p/Foxc1 pathway

Project description:Peritoneal dialysis (PD) is a successful renal replacement therapy for end-stage renal disease that effectively improves the quality of life. Long-term PD causes epithelial mesenchymal transformation (MMT) of peritoneal mesothelial cells, leading to peritoneal fibrosis which reduces the efficiency of PD. Macrophages are considered players in the onset and perpetuation of peritoneal injury. Yet, the mechanisms employed by macrophage-mesothelial cells communication to regulate peritoneal fibrosis are not fully elucidated resulting in lack of disease-modified drugs. This study analyzes the role of macrophage-mesothelial cell communication by intraperitoneal injection of macrophage derived exosomes in PD model rats. These results show that macrophages secrete exosomal miR-204-5p that directly targets Foxc1, leading to the activation of MMT in mesothelial cells. The data also shows that intraperitoneal injection of dissolved AS-IV can improve MMT by altering macrophage derived exosomal miRNAs. This study indicates that intercellular crosstalk between peritoneal macrophages and mesothelial cells is mediated by macrophage derived miR-204-5p-containing exosomes that control the MMT progression, providing AS-IV for prevention and treatment of PD induced peritoneal fibrosis. Our results demonstrate, for the first time, a novel role of the AS-IV on miR-204-5p/Foxc1/β-catenin axis in improving peritoneal fibrosis in vivo and vitro.

2023-01-01 | GSE165342 | GEO

Peritoneal cavity macrophage response to IFNg and IFNa

Project description:Peritoneal cavity macrophage response to IFNg and IFNa

| PRJNA433974 | ENA