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

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. We found that Oncostatin M (Osm), a member of the interleukin-6 cytokine superfamily secreted from Mincle-expressing macrophages, acts on fibroblasts to inhibit collagen expression.

ORGANISM(S): Mus musculus

PROVIDER: GSE285937 | 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_1]

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 | GSE276112 | GEO

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

2025-03-11 | GSE276113 | 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

Expression data from cancer associated fibroblasts (CAFs) treated with OSM

Project description:The cytokine Oncostatin M (OSM) promotes cancer progression by acting as central node for multicellular interactions between cancer cells and surrounding stromal cells. OSM is mainly secreted by myeloid cells and the oncostatin M receptor (OSMR) is expressed by cancer cells and cancer associated fibroblasts (CAFs), among others. To understand the effect of OSM in CAFs, a small and well-annotated Clariom S gene microarray was performed in CAF-173 cells cultured in 3D spheroids and treated with OSM or vehicle (PBS).

2022-02-02 | GSE195775 | GEO

Expression data from OSM-overexpressing and control MDA-MB-231 triple negative breast cancer cells

Project description:The cytokine Oncostatin M (OSM) promotes cancer progression by acting as central node for multicellular interactions between cancer cells and surrounding stromal cells. OSM is mainly secreted by myeloid cells and the oncostatin M receptor (OSMR) is expressed by cancer cells and cancer associated fibroblasts (CAFs), among others. To understand the effect of OSM in triple negative breast cancer cells, a small and well-annotated Clariom S gene microarray was performed in OSM-overexpressing (MDA-MB-231-hOSM) and control (MDA-MB-231-hC) MDA-MB-231 cells.

2022-02-02 | GSE195774 | GEO

Oncostatin M effects in IMR90 cells

Project description:The JAK2 mutation V617F is detectable in a majority of patients with Ph-negative myeloproliferative neoplasms (MPN). Enforced expression of JAK2 V617F in mice induces myeloproliferation and bone marrow (BM) fibrosis suggesting a causal role for the JAK2 mutant in the pathogenesis of MPN. However, little is known about mechanisms and effector molecules contributing to JAK2 V617F-induced myeloproliferation and fibrosis. Here we show that JAK2 V617F promotes expression of oncostatin M (OSM) in neoplastic myeloid cells. Correspondingly, OSM was found to be overexpressed in the BM and elevated in the serum of patients with JAK2 V617F+ MPN. In addition, OSM secreted by JAK2 V617F+ cells stimulated growth of fibroblasts and microvascular endothelial cells and induced the production of angiogenic and profibrogenic cytokines (HGF, VEGF, and SDF-1) in BM fibroblasts. All effects of MPN cell-derived OSM were blocked by a neutralizing anti-OSM antibody, whereas the production of OSM in MPN cells was effectively suppressed by a pharmacologic JAK2 inhibitor or RNAi-mediated knockdown of JAK2. In summary, JAK2 V617F-mediated upregulation of OSM may contribute to fibrosis, neoangiogenesis, and the cytokine storm observed in JAK2 V617F+ MPN, suggesting that OSM could serve as a novel therapeutic target molecule in these neoplasms. IMR90 cells were treated with a single dose of rh Oncostatin M (10ng/ml).

2013-01-29 | E-GEOD-29655 | biostudies-arrayexpress

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

Exercise-induced Crosstalk between Immune Cells and Adipocytes in Humans: Role of Oncostatin-M

Project description:The discovery of novel exercise-regulated circulatory factors has fueled interest in the role of organ-crosstalk, especially between skeletal muscle and adipose tissue in mediating beneficial effects of exercise. We studied the adipose tissue transcriptome in men and women with normal glucose tolerance or type 2 diabetes following an acute exercise bout, revealing substantial exercise and time-dependent changes, and a sustained increase in inflammatory genes unique to Type 2 diabetes. We identify Oncostatin-M as one of the most upregulated adipose tissue secreted factors post exercise. In cultured human adipocytes, oncostatin-M enhanced MAPK signalling and regulates lipolysis. Oncostatin-M expression predominantly arises from adipose tissue immune cell fractions, while the corresponding receptors are expressed in adipocytes. Oncostatin-M expression is induced in cultured human Thp1 macrophages in response to exercise-like stimuli. Our results suggest immune cells, via secreted factors such as oncostatin-M, are important in crosstalk between skeletal muscle and adipose tissue during exercise, to regulate adipocyte metabolism and adaptation.

2023-11-21 | GSE198922 | GEO

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