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Novel cell-to-cell communications between macrophages and fibroblasts regulate obesity-induced adipose tissue fibrosis [scRNA-seq_1]

ABSTRACT: Mincle (Macrophage inducible C-type lectin, clec4e) is a pattern recognition receptor expressed in innate immune cells and can sense cell death, suggesting a role in sterile inflammation. We previously showed that expression of Mincle is induced in adipose tissue macrophages during the development of obesity. Mincle accelerates adipose tissue inflammation and fibrosis, thereby exacerbating ectopic lipid accumulation and insulin resistance in the liver. In this study, we performed single-cell RNA sequencing analysis of the SVF in visceral adipose tissue from diet-induced obese mice to analyze the cell-cell interaction between Mincle-expressing macrophages and activated fibroblasts.

ORGANISM(S): Mus musculus

PROVIDER: GSE276112 | GEO | 2025/03/11

REPOSITORIES: GEO

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Novel cell-to-cell communications between macrophages and fibroblasts regulate obesity-induced adipose tissue fibrosis [scRNA-seq_2]

Project description:Mincle (Macrophage inducible C-type lectin, clec4e) is a pattern recognition receptor expressed in innate immune cells and can sense cell death, suggesting a role in sterile inflammation. We previously showed that expression of Mincle is induced in adipose tissue macrophages during the development of obesity. Mincle accelerates adipose tissue inflammation and fibrosis, thereby exacerbating ectopic lipid accumulation and insulin resistance in the liver. In this study, we performed single-cell RNA sequencing analysis of the SVF in visceral adipose tissue from diet-induced obese mice to analyze the cell-cell interaction between Mincle-expressing macrophages and activated fibroblasts.

2025-03-11 | GSE276113 | GEO

Novel cell-to-cell communications between macrophages and fibroblasts regulate obesity-induced adipose tissue fibrosis [bulk RNA-seq]

2025-03-11 | GSE285937 | GEO

Novel cell-to-cell communications between macrophages and fibroblasts regulate obesity-induced adipose tissue fibrosis [spatial transcriptomics]

Project description:Mincle (Macrophage inducible C-type lectin, clec4e) is a pattern recognition receptor expressed in innate immune cells and can sense cell death, suggesting a role in sterile inflammation. We previously showed that expression of Mincle is induced in adipose tissue macrophages during the development of obesity. Mincle accelerates adipose tissue inflammation and fibrosis, thereby exacerbating ectopic lipid accumulation and insulin resistance in the liver. In this study, we performed spatial transcriptomic analysis of the visceral adipose tissue from diet-induced obese mice to analyze distribution of Mincle-expressing macrophages and the gene expression around them.

2025-03-11 | GSE275590 | GEO

Expression data from peritoneal macrophages stimulated with trehalose-6,6'-dimycolate (TDM)

Project description:Macrophage-inducible C-type lectin (Mincle, Clec4e) is a pathogen sensor that recognizes pathogenic fungi and Mycobactrium tuberculosis. We perfomed microarray analysis using peritoneal macrophages stimulated with TDM, a mycobacterial cell wall glycolipid that is known to be a Mincle ligand. Many chemokine and cytokine genes were upregulated in wildtype macrophages stimulated with TDM. Upregulation of these genes were completely abolishd in Mincle KO macrophages. Peritoneal macrophages from WT and Mincle KO mice were stimulated with TDM or vehicle for 24 h (3 samples each). Microarray analysis was performed using Affymetrix Mouse 430 2.0.

2013-11-14 | E-GEOD-52338 | biostudies-arrayexpress

Expression data from peritoneal macrophages stimulated with trehalose-6,6'-dimycolate (TDM)

2013-11-14 | GSE52338 | GEO

Single-cell sequencing reveals Mincle receptor mediated inflammation for resolution in ischemic kidney injury

Project description:Recent studies have demonstrated a strong association between acute kidney injury (AKI) and chronic kidney disease (CKD), while the unresolved inflammation is believed to be a driving force for this chronic transition process. As a transmembrane pattern recognition receptor, Mincle (macrophage-inducible C-type lectin, Clec4e) was identified to participate in the early immune response after AKI. However, the impact of Mincle on the chronic transition of AKI remains largely unclear. We performed single-cell RNA sequencing (scRNA-seq) with the unilateral ischemia-reperfusion (UIR) murine model of AKI at days 1, 3, 14 and 28 after injury. Potential effects and mechanism of Mincle on renal inflammation and fibrosis were further validated in vivo utilizing Mincle knockout mice. The dynamic expression of Mincle in macrophages and neutrophils throughout the transition from AKI to CKD was observed. For both cell types, Mincle expression was significantly up-regulated on day 1 following AKI, with a second rise observed on day 14. Notably, we identified distinct subclusters of Mincle-high neutrophils and Mincle-high macrophages that exhibited time-dependent influx with dual peaks characterized with remarkable pro-inflammatory and pro-fibrotic functions. Moreover, we identified that Mincle-high neutrophils represented an "aged" mature neutrophil subset derived from the "young" mature neutrophil cluster in kidney. Additionally, we observed a synergistic mechanism whereby Mincle-expressing macrophages and neutrophils sustained renal inflammation by augmenting tumor necrosis factor (TNF) production. Mincle-deficient mice exhibited reduced renal injury and fibrosis following AKI.

2024-05-23 | GSE267242 | GEO

The role of Clec4e (Mincle) in microglia response to transient ischemic injury

Project description:This data set shows dramatic changes in gene expression in microglia isolated from C57Bl6/J mice subjected to transient middle cerebral artery occlusion, as compared to those subjected to sham surgery. Mice deficient in Mincle (Clec4e-/-) showed significantly improved injury outcomes 3 and 7 days after transient middle cerebral artery occlusion. However, when comparing changes in gene expression in microglia 24 hours after blood reperfusion, there were no differences between wild-type and Clec4e-/- mice, indicating that Mincle does not participate in early microglial activation. Wild type and Mincle knock-out (Clec4e-/-) mice. After 1 h of transient middle cerebral artery occlusion (tMCAO) and 24 h of reperfusion, mice were perfused with PBS, their brains dissected, and 2 ipsilesional hemispheres (with cerebellum and brainstem removed) pooled for microglia isolation. For sham-operated animals, the whole forebrain was used and brains were not pooled. After myelin separation by Percoll gradient centrifugation, around 80,000 CD45intermediate, CD11b+ microglial cells were sorted from each sample. Sham samples n=3, tMCAO samples n=5.

2016-03-24 | E-GEOD-77986 | biostudies-arrayexpress

The role of Clec4e (Mincle) in microglia response to transient ischemic injury

2016-03-24 | GSE77986 | GEO

Microbiota exposure following DSS-induced colitis promotes Mincle-mediated training of myeloid progenitors

Project description:Impairment of the intestinal barrier allows the systemic translocation of commensal bacteria, inducing a pro-inflammatory state in the host. To explore this link, we investigated innate immune responses following increased gut permeability upon administration of dextran sulfate sodium (DSS) in mice. We found that microbiota translocation induced trained immunity (TI) in mouse myeloid bone marrow progenitors (BMPs). Enterococcus faecalis was isolated from bone marrow following DSS treatment and induced trained immunity hallmarks in bone marrow-derived mouse macrophages and human monocytes. Notably, DSS treatment or heat-killed E. faecalis reprogrammed BMPs, resulting in enhanced inflammatory responses in vitro and in vivo, and protection against pathogen infections. The C-type lectin receptor Mincle (Clec4e) was essential for E. faecalis-induced TI in BMPs. Clec4e-/- mice showed impaired TI upon E. faecalis and reduced pathology following DSS treatment. Thus, Mincle sensing of E. faecalis induces TI that may contribute to pathologies associated with increased gut permeability. This SuperSeries is composed of the SubSeries listed below.

2025-01-22 | GSE281377 | GEO

RNA sequencing of the stomachs of H. pylori-infected WT and Mincle–/– mice after 8 weeks

Project description:Helicobacter pylori (H. pylori) causes assorted gastrointestinal disorders. H. pylori-specific T cells develop during infection, which is a prerequisite for the induction of gastritis and malignancy. How the innate immune system senses H. pylori to prime T cells remains unclear. We report that cholesteryl glucosides in H. pylori activate innate immunity through C-type lectin receptors (CLRs). Cholesteryl acyl α-glucoside (αCAG) was identified as a ligand for Mincle (Clec4e). Upon H. pylori infection, T cell responses and gastritis were ameliorated in Mincle-deficient mice, although bacterial numbers were comparable.Thus the cholesteryl lipid–CLR axis exacerbates H. pylori-induced gastric inflammation with limited contribution to protective immunity.

2020-09-19 | GSE136203 | GEO

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