Gene expression in cardiac macrophages
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE53787 | GEO | 2014/01/18
SECONDARY ACCESSION(S): PRJNA235896
REPOSITORIES: GEO
Similar Datasets
Project description:Three cardiac macrophage subsets and blood ly6chi monocytes were sorted to compare gene expression at steady state. 4 samples (CCR2+ Mac, MHC-IIlo Mac, MHC-IIHi Mac, Ly6cHi Mono), with 4 replicates of each sample.
2014-01-18 | E-GEOD-53787 | biostudies-arrayexpress
Project description:Two types of monocytes, inflammatory and patrolling, infiltrate the hearts in both human myocarditis and murine experimental autoimmune myocarditis (EAM) model. The fates and functions of these infiltrating monocytes governing the progression of heart failure remain unclear. Here, we created parabiotic EAM and naïve mice to show that cardiac inflammation facilitate monocyte-to-macrophage differentiation. Using a combination of flow cytometry, time lapsed imaging and transmission electron microscopy, we demonstrated in vitro that cardiac fibroblasts interact with monocytes and are instrumental in facilitating monocyte-to-macrophage differentiation. Moreover, IL-17A stimulated cardiac fibroblasts completely arrested Ly6Clo monocyte proliferation and inhibited both Ly6Chi and Ly6Clo monocyte-to-macrophage differentiation both in vitro and in vivo after intracardiac injections of monocytes into the hearts. Intriguingly, IL-17A signaling through cardiac fibroblasts also significantly downregulated Mer tyrosine kinase (MerTK) expressions on Ly6Chi monocyte-derived macrophages, thus jeopardizing their phagocytic abilities. Collectively, our results implicate divergent fates and functions of heart-infiltrating monocytes influenced by cardiac fibroblasts.
2021-08-01 | GSE118861 | GEO
Project description:Mononuclear phagocytes promote injury and repair following myocardial infarction but discriminating functions within mixed populations remains challenging. We utilized fate mapping and single cell RNA-sequencing to delineate fate specification trajectories of heterogeneous cardiac macrophage subpopulations. In steady state, TIMD4 expression tracked with a dominant resident cardiac macrophage subset that persisted via in situ self-renewal with minimal monocyte input. Following ischemic injury, monocytes displayed significant plasticity, ultimately adopting transcriptional states similar to resident macrophages, but also multiple unique states. Ischemic injury reduced resident macrophage abundance within infarct tissue, and despite transcriptional similarity, TIMD4 expression distinguished resident from recruited macrophages. Specific lineage-based depletion of resident cardiac macrophages resulted in depressed cardiac function and adverse remodeling primarily within the peri-infarct zone, the only region of the myocardium where resident macrophages expanded numerically following injury. Together, these data highlight a non-redundant, cardioprotective role of resident cardiac macrophages, and the diverse transcriptional fates recruited monocytes can adopt.
2018-12-15 | GSE119355 | GEO
Project description:Purpose: In our study, we identified a heterogeneity among bone marrow (BM) Ly6Chi monocytes, which can be subdivided the expression of CXCR4. In order to understand the development of BM monocytes, the goal of this experiment is to compare the transcriptome of these 2 BM Ly6Chi monocyte subsets to those of the common monocyte progenitor (cMoP) and Ly6Clo monocytes.
2016-09-29 | GSE86079 | GEO
Project description:To compare the gene expression profiles of Macrophage & Dendritic cell Progenitors (MDPs), Common Dendritic cell Progenitors (CDPs), committed dendritic cell precursors (pre-DCs), and Ly6Chi monocytes from mouse bone marrow Four samples (MDPs, CDPs, pre-DCs, and monocytes) were collected in triplicate
2012-04-25 | E-GEOD-37566 | biostudies-arrayexpress
Project description:Monocytes are integral cells of the innate immune system that play important roles in host defence and tissue repair. It is well established that monocytes are derived from the common monocyte progenitor (cMoP) in the bone marrow (BM) before giving rise to Ly6Chi mature monocytes that enter the circulation. However, our lab has discovered that BM Ly6Chi monocytes are not homogenous, and consist of two subpopulations (CXCR4hi and CXCR4lo) in both mice and humans. In particular, the CXCR4hi subset (termed transitional pre-monocyte (TpMo) population) actively proliferates in the BM and matures into the CXCR4lo subset, which represents mature Ly6Chi monocytes. Nevertheless, how this TpMo population may behave beyond their precursor role in the BM remains undefined. While TpMos have been shown to be strictly immobilized in the BM in the steady state, our preliminary data revealed the mobilization of TpMos into the circulation during sepsis. Furthermore, TpMos were found to give rise to more macrophages than mature Ly6Chi monocytes. Our data hence suggests a critical peripheral role for TpMos that may implicate the outcome of sepsis and possible potential implications in future therapies associated with monocytes. Based on our preliminary findings, we aim to have a better understanding of these monocyte subsets and how they are transcriptionally distinct when they have become macrophages. In particular, we would like to determine if TpMo-derived macrophages are less inflammatory compared to mature monocyte-derived macrophages.
2022-03-09 | GSE192449 | GEO
Project description:To compare the gene expression profiles of Macrophage & Dendritic cell Progenitors (MDPs), Common Dendritic cell Progenitors (CDPs), committed dendritic cell precursors (pre-DCs), and Ly6Chi monocytes from mouse bone marrow
2012-04-26 | GSE37566 | GEO
Project description:Analysis of Ly6Chi monocytes from small intestine lamina propria (SILP) and blood of day 8 Toxoplasma gondii infected mice at gene expression level. The hypothesis tested in the present study was that Ly6Chi monocytes from SILP have altered expression of regulatory factors to blood monocytes. Results provide important information on the regulatory to effector balance of genes expressed by Ly6Chi monocytes during an acute inflammatory response. Ly6Chi inflammatory monocytes were sorted by FACS from the blood or small intestine lamina propria (SILP) of Toxoplasma gondii infected C57BL/6 mice. Cells were isolated at day 8 after infection and total RNA obtained from sorted populations. Three biological replicates were acquired for both blood and SILP from pooled animals.
2013-05-25 | E-GEOD-46685 | biostudies-arrayexpress
Project description:We studied the role of Notch2 signaling in Ly6Chi monocyte cell fate during TLR7-induced acute inflammation. To characterize the gene expression changes involved in monocyte differentiation, we subjected monocyte subsets from peripheral blood of wt and myeloid Notch2 mutant mice after Sham or IMQ treatment to RNA-sequencing and gene expression analysis. We found that Cell-intrinsic Notch2 and TLR7-Myd88 pathways independently and synergistically promote Ly6Clo patrolling monocyte development from Ly6Chi monocytes under inflammatory conditions. At the same time TLR7 stimulation in the absence of functional Notch2 signaling promotes resident tissue macrophage gene expression signatures in monocytes and ectopic differentiation of Ly6Chi monocytes into macrophages and dendritic cells. Thus, Notch2 is a master regulator of Ly6Chi monocyte cell fate and inflammation in response to TLR signaling.
2020-08-04 | GSE147492 | GEO
Project description:Transcription profiling by array of Mrc1+ cardiac tissue macrophage subsets to identify deferentially expressed genes.
2014-08-04 | E-MTAB-2168 | biostudies-arrayexpress