Visceral adipose tissue macrophage subsets
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE118226 | GEO | 2020/08/07
REPOSITORIES: GEO
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Project description:Visceral adipose tissue macrophage subsets
| PRJNA484897 | ENA
Project description:Background: The onset, progression, and outcomes of myocardial infarction (MI), a serious issue worldwide, are regulated by inflammatory responses. Numerous studies have demonstrated the complexity and importance of post-infarction immunity. Nonetheless, little is known about dynamic changes in cell type and function during disease progression. Methods: Single-cell RNA sequencing (scRNA-seq) was used to map the Cd45+ immune cell composition at different time points (0, 3, 7 and 14 days) after MI within a mouse left anterior descending coronary artery (LAD) ligation model. A time course-analysis was performed to characterize dynamic changes in cell populations. Multiparameter flow cytometry, immunohistochemistry, and immunofluorescence were performed using the same mouse model. Results: Major immune cell populations, distinct subsets, and dynamic changes were identified. Macrophages (Mø)/monocytes were most abundant, peaking at 3 days after infarction. Mø-5 and Mø-6 were the predominant infiltrated subsets at this time point, with strong expression of inflammatory factors. Further analysis demonstrated that suppressing these sets attenuated pathological MI progression by preventing subsequent leukocyte extravasation and adverse remodeling. We also detected abundant apoptotic neutrophils and a profibrotic macrophage subset on days 7 and 14 respectively. Conclusions: Our results provide a basis for developing cell type- and time-specific interventions in MI.
2022-01-11 | GSE163465 | GEO
Project description:Myocardial infarction (MI) causes sterile inflammation, which is characterized by recruitment and activation of innate and adaptive immune system cells. We have delineated the temporal dynamics of immune cell accumulation following MI by flow cytometry. Macrophages were numerically the predominant cells infiltrating the infarcted myocardium, increasing in number over the first week post-MI. Macrophages are functionally heterogeneous, and can be classified into M1 and M2 macrophages, respectively, based on surface-marker expression. M1 macrophages dominated at 1-3 days post-MI, whereas M2 macrophages represented the predominant macrophage subset after 5 days. We used microarrays to examine the gene expression profiles of the macrophages sorted from the hearts at different timepoints after MI. We identified the kinetics of gene expression of cardiac macrophage after MI.
2017-03-27 | GSE88924 | GEO
Project description:Myocardial infarction (MI) results from occlusion of blood supply to the heart muscle causing death of cardiac muscle cells. Following myocardial infarction (MI), scar formation acts to mechanically stabilise the injured heart to prevent rupture and death. While fibroblasts and macrophages are implicated in post-MI scar formation and maturation, their exact contributions to this process are poorly characterised, especially in the long-term (i.e., beyond 1-week post-MI). Here, we employ state-of-the-art spatially-targetted optical micro-proteomics (STOMP) to isolate proteomes of tissue fractions enriched for fibroblasts (sma+) and macrophages (cd68+) over a 6-week post-MI timecourse and compare them to whole-scar proteome. We illustrate dynamic, specific changes in sma- and cd68-enriched fraction protein composition over 1-6 weeks post-MI with some of these changes reflected in whole-infarct preparations. These results link specific cell populations to specific protein changes in whole infarct.
2023-10-31 | PXD034413 | Pride
Project description:Sterile tissue injury is thought to locally activate innate immune responses via damage associated molecular patterns (DAMPs). Whether innate immune pathways are remotely activated remains relatively unexplored. Here, by analyzing ~145,000 single cell transcriptomes at steady state and after myocardial infarction (MI) in mice and humans, we show that the type I interferon (IFN) response, characterized by expression of interferon stimulated genes (ISGs), begins far from the site of injury, in neutrophil and monocyte progenitors within the bone marrow. In the peripheral blood of patients, we observed defined subsets of ISG-expressing neutrophils and monocytes. In the bone marrow and blood of mice, ISG expression was detected in neutrophils and monocytes and their progenitors; intensified with maturation at steady-state and after MI; and was dependent on Tet2 and Irf3 transcriptional regulators. Within the infarcted heart, ISG-expressing cells were negatively regulated by Nrf2-activation in Ccr2- steady-state cardiac macrophages. Our results show that IFN signaling begins in the bone marrow, implicate multiple transcription factors in its regulation (Tet2, Irf3, Nrf2), and provide a clinical biomarker (ISG score) for studying IFN signaling in patients.
2020-09-12 | GSE157244 | GEO
Project description:The specific mechanism of sodium-glucose cotransporter 2 (SGLT2) inhibitor in heart failure (HF) needs to be elucidated. In this study, we use SGLT2 global knockout (SGLT2-KO) mice to assess the mechanism of SGLT2 inhibitor on HF. Dapagliflozin ameliorates both myocardial infarction (MI)-and transverse aortic constriction (TAC) -induced HF. Global SGLT2-deficiency doesn’t exert protection against adverse remodeling in both MI- and TAC-induced HF models. Dapagliflozin blurs MI- and TAC-induced HF phenotypes in SGLT2-KO mice. Dapagliflozin causes major changes in cardiac fibrosis and inflammation. Based on single-cell RNA sequencing dapagliflozin causes significant differences in the gene expression profile of macrophages and fibroblasts. Moreover, dapagliflozin directly inhibites macrophage inflammation, thereby suppressing cardiac fibroblasts activation. The cardio-protection of dapagliflozin is blurred in mice treated with a C-C chemokine receptor type 2 (CCR2) antagonist. Taken together the protective effects of dapagliflozin against HF are independent of SGLT2, macrophage inhibition is the main target of dapagliflozin against HF.
2023-11-14 | GSE247062 | GEO
Project description:Characterisation of M2-like macrophage in terms of gene expression level. The hypothesis tested in the present study was that M2-like macrophages in myocardial infarction (MI) heart have upregulation of genes relevant to cardiac repair. The results obtained showed tha various tanti-inflammatory and reparative genes were upregulated in M2-like macrophage from MI heart compared to those from intact hearts. M2-like macrophages from the heart (either MI or intact) were distinct from those in the peritoneal cavity.
2017-06-14 | GSE69879 | GEO
Project description:Kidney macrophages are comprised of both monocyte-derived and tissue resident populations; however, the heterogeneity of kidney macrophages and factors that regulate their heterogeneity are poorly understood. Herein, we performed single cell RNA sequencing (scRNAseq), fate mapping, and parabiosis to define the cellular heterogeneity of kidney macrophages in healthy mice. Our data indicate that healthy mouse kidneys contain four major subsets of monocytes and two major subsets of kidney resident macrophages (KRM) including a population with enriched Ccr2 expression, suggesting monocyte origin. Surprisingly, fate mapping data using the newly developed Ms4a3Cre Rosa Stopf/f TdT model indicate that less than 50% of Ccr2+ KRM are derived from Ly6chi monocytes. Instead, we find that Ccr2 expression in KRM reflects their spatial distribution as this cell population is almost exclusively found in the kidney cortex. We also identified Cx3cr1 as a gene that governs cortex specific accumulation of Ccr2+ KRM and show that loss of Ccr2+ KRM reduces the severity of cystic kidney disease in a mouse model where cysts are mainly localized to the kidney cortex. Collectively, our data indicate that Cx3cr1 regulates KRM heterogeneity and niche-specific disease progression.
2023-05-01 | GSE193892 | GEO
Project description:Myocardial infarction (MI) leads to cardiomyocyte death, which triggers an immune response that clears debris and restores tissue integrity. In the adult heart, the immune system facilitates scar formation, which repairs the damaged myocardium but compromises cardiac function. In neonatal mice, the heart can regenerate fully without scarring following MI; however, this regenerative capacity is lost by P7. The signals that govern neonatal heart regeneration are unknown. By comparing the immune response to MI in mice at P1 and P14, we identified differences in the magnitude and kinetics of monocyte and macrophage responses to injury. Using a cell-depletion model, we determined that heart regeneration and neoangiogenesis following MI depends on neonatal macrophages. Neonates depleted of macrophages were unable to regenerate myocardia and formed fibrotic scars, resulting in reduced cardiac function and angiogenesis. Immunophenotyping and gene expression profiling of cardiac macrophages from regenerating and nonregenerating hearts indicated that regenerative macrophages have a unique polarization phenotype and secrete numerous soluble factors that may facilitate the formation of new myocardium. Our findings suggest that macrophages provide necessary signals to drive angiogenesis and regeneration of the neonatal mouse heart. Modulating inflammation may provide a key therapeutic strategy to support heart regeneration. Total RNA was isolated from CD11b+Ly6G- cells sorted from hearts 3 days following ligation of LAD. 6 samples total: Triplicates of cells from P1 mice and from P14 mice
2014-01-31 | E-GEOD-54530 | biostudies-arrayexpress
Project description:Thyroid hormone improves left ventricular remodeling and cardiac performance after myocardial infarction (MI), but the molecular basis is unknown. This study was designed to detect gene expression changes in left ventricular non-infarcted areas at 4 weeks following myocardial infarction with and without thyroid hormone treatment. The results suggest that altered expression of genes for molecular function and biological process may be involved in the beneficial effects of thyroid hormone treatment following myocardial infarction in rats. MI was produced by ligation of the left anterior descending coronary artery in female SD rats. Rats were divided into the following groups: (1) Sham MI, (2) MI, and (3) MI+T4 treatment (T4 pellet 3.3mg, 60 days release, implanted subcutaneously immediately following MI). Four weeks after surgery, total RNA was isolated from left ventricular non-infarcted areas for microarray analysis using the Illumina RatRef-12 Expression BeadChip Platform.
2012-04-30 | E-GEOD-35088 | biostudies-arrayexpress