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Expression data from Aortic Macrophages

ABSTRACT: Normal arteries contain a large population of tissue resident macrophages (MΦ). Their origins, as well as the mechanisms that sustain them during homeostasis and disease, however, are poorly understood. Gene expression profiling, we show, identifies arterial MΦ as a distinct population among tissue MΦ. Ontologically, arterial MΦ arise before birth, though CX3CR1-, Csf1r-, and Flt3-driven fate mapping approaches demonstrate MΦ colonization occurs through successive contributions of yolk sac (YS) and conventional hematopoiesis. In adulthood, arterial MΦ renewal is driven by local proliferation rather than monocyte recruitment from the blood. Proliferation sustains MΦ not only during steady state conditions, but mediates their rebound after severe depletion following sepsis. Importantly, the return of arterial MΦ to functional homeostasis after infection is rapid; repopulated MΦ exhibit a transcriptional program similar to resting MΦ and efficiently phagocytose bacteria. Collectively, our data provide a detailed framework for future studies of arterial MΦ function in health and disease.

ORGANISM(S): Mus musculus

PROVIDER: GSE68968 | GEO | 2015/12/07

SECONDARY ACCESSION(S): PRJNA284232

REPOSITORIES: GEO

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Expression data from Aortic Macrophages

Project description:Normal arteries contain a large population of tissue resident macrophages (MÎ¦). Their origins, as well as the mechanisms that sustain them during homeostasis and disease, however, are poorly understood. Gene expression profiling, we show, identifies arterial MÎ¦ as a distinct population among tissue MÎ¦. Ontologically, arterial MÎ¦ arise before birth, though CX3CR1-, Csf1r-, and Flt3-driven fate mapping approaches demonstrate MÎ¦ colonization occurs through successive contributions of yolk sac (YS) and conventional hematopoiesis. In adulthood, arterial MÎ¦ renewal is driven by local proliferation rather than monocyte recruitment from the blood. Proliferation sustains MÎ¦ not only during steady state conditions, but mediates their rebound after severe depletion following sepsis. Importantly, the return of arterial MÎ¦ to functional homeostasis after infection is rapid; repopulated MÎ¦ exhibit a transcriptional program similar to resting MÎ¦ and efficiently phagocytose bacteria. Collectively, our data provide a detailed framework for future studies of arterial MÎ¦ function in health and disease. Aortic macrophages (CD11bhighF4/80highCD45+MerTK+CD64+) were isolated from C57/B6 wild-type male mice aged 6-8 weeks before and 7 days after induction of sepsis by cecal puncture. 18-20 aortas were pooled per sample. Each condition contained three biological replicates.

2015-12-07 | E-GEOD-68968 | biostudies-arrayexpress

Hemogenic endothelial fate mapping reveals dual developmental origin of mast cells.

Project description:Hematopoiesis occurs in distinct waves. ‘Definitive’ hematopoietic stem cells (HSC) with the potential for all blood lineages emerge in the aorta-gonado-mesonephros (AGM), while ‘primitive’ progenitors, whose potential is thought to be limited to erythrocytes, megakaryocytes and macrophages (MΦ), arise earlier in the yolk sac (YS). Here, we questioned whether other YS lineages exist that have not been identified, partially owing to limitations of current lineage tracing models. We established the use of Cdh5CreERT2 for hematopoietic fate mapping, which revealed the YS origin of mast cells (MC). YS derived MC are replaced by definitive MC, which maintain themselves independently from the BM in the adult. Replacement occurs with tissue specific kinetics. MC in the skin, but not other organs, remain largely YS derived prenatally and are phenotypically and transcriptomically distinct from definite adult MC. We conclude that dual hematopoietic origin is not MΦ specific, but shared between these two myeloid lineages.

2018-06-01 | GSE104790 | GEO

iPSC-derived macrophages effectively treat pulmonary alveolar proteinosis in Csf2rb-deficient mice

Project description:The key aim of this experiment is to characterize the iPSC-Mφ population before and after pulmonary transplantation. For this purpose the following cell populations were compared: (i) transplanted iPSC-Mφ, (ii) Mφ obtained by in vitro differentiation of murine lineage-negative bone marrow cells (BM-Mφ), (iii) non-differentiated CD45.1 iPSC, (iv) murine alveolar Mφ (AMφ) isolated from the BALF of healthy control mice, and (v) iPSC-Mφ recovered from the transplanted animals two months after (PMT-Mφ).

2018-07-10 | E-MTAB-6442 | biostudies-arrayexpress

Adult-repopulating lymphoid potential is not confined to the arterial endothelial cells in yolk sac

Project description:During embryogenesis, hematopoietic stem progenitor cells (HSPCs) are believed to be derived from hemogenic endothelial cells (HECs). Moreover, arterial feature is proposed to be a prerequisite for the HECs to generate HSPCs with lymphoid potential. Whereas the molecular basis of the hematopoietic stem cell-competent HECs has been delicately elucidated within the embryo proper, the functional and molecular heterogeneity of HECs in the extra-embryonic yolk sac (YS) remains largely unresolved. In this study, we firstly identified six molecularly different endothelial populations in the mid-gestational YS through integrated analysis of several single-cell RNA sequencing (scRNA-seq) datasets, and validated the arterial vasculature distribution of Gja5+ ECs by using a Gja5-EGFP reporter mouse model. We further explored the hemogenic potential of different EC populations based on their Gja5- EGFP and CD44 expression. The lineage differentiation potentials of ECs were spatiotemporally different and the B lymphoid potential was detected in the YS ECs as early as embryonic day (E) 8.5 regardless of their arterial feature. Unexpectedly, capacity of generating hematopoietic progenitors with in vivo lymphoid potential was found in non-arterial in addition to arterial YS ECs at E10.0-E10.5. Importantly, the distinct identities of E10.0-E10.5 ECs with a hemogenic potential between those from YS and from intra-embryonic caudal region were revealed by further scRNA-seq analysis. Taken together, these findings extend our knowledge about the hemogenic potential of ECs from anatomically and molecularly different vascular beds, providing a theoretical basis for better understanding the sources of HSPCs during mammalian development.

2021-07-12 | GSE167588 | GEO

Role of transcriptional coregulator GRIP1 in control of macrophage polarization and metabolic homeostasis

Project description:Diet-induced obesity is characterized by macrophage (MΦ) infiltration and low-grade chronic inflammation in white adipose tissue (WAT) leading to insulin resistance. WAT MΦ are highly heterogeneous in their origin, patterns of gene expression and activities: unlike infiltrating monocyte-derived MΦ that promote inflammation and metabolic dysfunction, tissue-resident WAT MΦ originally described as ‘M2’ are phenotypically anti-inflammatory and counteract obesity and insulin resistance. Despite the critical role of the balance between these MΦ populations in metabolic homeostasis, the molecular mechanisms and key players that establish the resident MΦ transcription program are poorly understood. We recently reported that glucocorticoid receptor (GR)-interacting protein (GRIP)1 - a nuclear receptor coactivator - cooperates with GR to repress transcription of inflammatory genes. Here, using mice conditionally lacking GRIP1 in MΦ (cKO), we show that GRIP1 promotes MΦ polarization in response to IL4 (M2(IL4)) via a nuclear receptor-independent pathway by serving as a coactivator for Kruppel-like factor (KLF)4 – a critical driver of tissue MΦ differentiation. Interestingly, in vivo, GRIP1 cKO mice challenged with high-fat diet develop massive MΦ infiltration and chronic inflammation in WAT and liver, fatty livers, hyperglycemia, hyperinsulinemia and glucose intolerance consistent with metabolic syndrome phenotype. Together, our findings identify GRIP1 as a critical regulator of immunometabolism, which relies on distinct transcriptional mechanisms to coordinate the balance between MΦ populations in vivo thereby protecting mice from obesity-induced metabolic disease.

2017-02-07 | GSE80160 | GEO

Induced pluripotent stem cell-derived primitive macrophages as a cellular platform to model tissue-resident macrophage differentiation and function

Project description:Specialized tissue macrophages arise during embryogenesis from yolk-sac (YS) progenitors that migrate into developing tissues and terminally differentiate in situ. Until recently, it has been impossible to isolate or derive sufficient numbers of YS-derived macrophages for further study, but data now suggest that induced pluripotent stem cells (iPSCs) can be driven to undergo a process reminiscent of YS-hematopoiesis in vitro. We asked whether iPSC-derived primitive macrophages (iMac) can terminally differentiate into specialized macrophages using growth factors and organ-specific cues. Co-culturing murine iMac with iPSC-derived neurons promoted differentiation into microglia-like cells in vitro. Furthermore, murine iMac differentiated in vivo into microglia following injection into the brain, and functional alveolar macrophages after engraftment in the lung.

2017-07-20 | GSE99078 | GEO

NCX1 represents an ionic Na+ sensing mechanism in macrophages

Project description:Inflammation and infection can trigger local tissue Na+-accumulation. This Na+-rich environment boosts pro-inflammatory activation of monocyte/macrophage-like cells (MΦ) and their antimicrobial activity. Enhanced Na+-driven MΦ-function requires the osmoprotective transcription factor nuclear factor of activated T cells 5 (NFAT5), which augments NO production and contributes to increased autophagy. However, the mechanism of Na+-sensing in MΦ remained unclear. High extracellular Na+ levels (HS) trigger a substantial Na+-influx and Ca2+ loss. Here, we show that the Na+/ Ca2+-exchanger 1 (NCX1/ solute carrier family 8 member A1 (SLC8A1)) plays a critical role in HS-triggered Na+-influx, concomitant Ca2+ efflux and subsequent NFAT5 accumulation. Moreover, interfering with NCX1-activity impairs HS-boosted inflammatory signaling, infection-triggered autolysosome formation and subsequent antibacterial activity. Taken together, this demonstrates that NCX1 is able to sense Na+ and is required for amplifying inflammatory and antimicrobial MΦ responses upon HS exposure. Manipulating NCX1 offers a new strategy to regulate MΦ function.

2020-06-29 | GSE136662 | GEO

Fetal monocytes possess increased metabolic capacity and replace primitive macrophages in tissue macrophage development

Project description:We studied alveolar macrophage (AM) development after single and competitive transplantation of different precursors from YS, fetal liver, and lung into neonatal Csf2ra-/- mice, which lack endogenous AM. Fetal monocytes, promoted by Myb, outcompeted primitive MΦ (pMΦ) in empty AM niches and preferentially developed to mature AM, which is associated with enhanced mitochondrial respiratory and glycolytic capacity and repression of the transcription factors c-Maf and MafB. Interestingly, AM derived from pMΦ failed to efficiently clear alveolar proteinosis and protect from fatal lung failure following influenza virus infection. Thus, our data demonstrate superior developmental and functional capacity of fetal monocytes over pMΦ in AM development and underlying mechanisms explaining replacement of pMΦ in fetal tissues.

2019-12-30 | GSE140645 | GEO

RNAseq data of brain cortex from mice at d10 post-microglia depletion and non-depleted controls

Project description:Previous studies have reported that microglia depletion leads to impairment of synapse formation and these cells rapidly repopulate from CNS progenitors. However, the impact of microglia depletion and repopulation on the long-term state of the CNS environment has not been characterized. Here, we found by RNA-seq analysis that acute and synchronous microglia depletion results in a type 1-interferon inflammatory signature in degenerating somatosensory cortex in microglia-depleted mice. Transcriptomic and mass cytometry analysis of repopulated microglia demonstrates an interferon regulatory factor 7-driven activation state. Minocycline and anti-IFNAR1 antibody treatment attenuate the CNS type-1 interferon-driven inflammation and restore microglia homeostasis. Together, we found that acute microglia ablation induces a type-1 interferon activation state of grey matter microglia associated with acute neurodegeneration.

2018-06-08 | GSE115447 | GEO

T cell zone resident macrophages silently dispose of apoptotic cells in the lymph node

Project description:Dendritic cells (DC) are the most potent antigen-presenting cells of the immune system. In lymph nodes (LN), they are also believed to dispose of apoptotic cells, a critical function usually achieved by macrophages (Mφ) in other tissues. We report a population of tolerogenic Mφ located in the T cell zone of LN. T zone Mφ (TZM) are long lived Mφ seeded after birth and slowly replaced by blood monocytes. We show that TZM but not DC act as the only professional scavengers clearing apoptotic cells in the LN T cell zone. Importantly, we demonstrate that TZM prevent the capture of apoptotic cells by DC and the associated potential noxious activation of T cell immunity. We thus propose a new model in which efferocytosis and T cell activation are uncoupled processes handled by TZM and DC respectively.

2017-08-21 | GSE93592 | GEO

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