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RNA sequencing data of CNS-associated macrophages (CAMs) isolated from brains of Mrc1-CreERT2 mice

ABSTRACT: RNA sequencing data of CNS-associated macrophages (CAMs) isolated from brains of Mrc1-CreERT2 mice

PROVIDER: PRJNA800644 | ENA |

REPOSITORIES: ENA

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RNA sequencing data of CNS-associated macrophages (CAMs) isolated from brains of Mrc1-CreERT2 mice

Project description:All tissue resident macrophages of the central nervous system (CNS), including parenchymal microglia as well as CNS-associated macrophages (CAMs) such as meningeal (mMF) and perivascular macrophages (pvMF) are part of the CNS endogenous innate immune system that acts as the first line of defense during infections or trauma. It has been suggested that microglia and all CAM subsets are derived from prenatal cellular sources in the yolk sac that were defined as early erythromyeloid progenitors. However, the precise ontogenetic relationships, the underlying transcriptional programs and the molecular signals that drive the development of distinct CAMs subsets in situ are poorly understood. Using novel fate mapping systems, single-cell profiling and cell-specific mutants, we show that only mMF and microglia share a common prenatal progenitor. In contrast, pvMF originate from perinatal mMF only after birth in an integrin-dependent manner. Furthermore, the establishment of pvMF critically requires the presence of vascular smooth muscle cells. In summary, our data reveal a novel precisely timed process in distinct anatomical niches for the establishment of CNS macrophage subsets.

2022-01-27 | GSE194433 | GEO

RNA sequencing data of microglia isolated from brains of WT, Hexb-tdTomato, Hexb-CreERT2 and Hexb-KO mice. {Reporter]

Project description:RNA sequencing of FACS sorted microglia isolated from brain tissue of WT, Hexb-tdTomato, Hexb-CreERT2 and Hexb-KO mice was performed to test for potential differences in gene expression caused by the knock-in of tdTomato and CreERT2 into the Hexb locus.

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RNA sequencing data of microglia isolated from brains of WT, Hexb-tdTomato, Hexb-CreERT2 and Hexb-KO mice. [Cre]

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RNA sequencing data of microglia isolated from brains of WT, Hexb-tdTomato, Hexb-CreERT2 and Hexb-KO mice. [Hexb-KO]

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Immunotyping of microglia and macrophages in the CNS during acute SIV infection: a single-cell study of rhesus macaque brains

Project description:Human immunodeficiency virus (HIV) is widely recognized for its striking impact on the immune system. Even though HIV is primarily known for the impairment of the peripheral CD4 T cells, its influence on the central nervous system (CNS) also cannot be neglected. The main immune constituents in the brain, microglia and macrophages, are the target for HIV in the brain, as well as for the simian immunodeficiency virus (SIV) in nonhuman primates. This infection can lead to neurological effects as well as the establishment of a virus reservoir. Given the gaps in our knowledge on how these cells respond in vivo to CNS infection, we performed single-cell RNA sequencing (scRNA-seq) on myeloid cells from the brains of 3 rhesus macaque with 12-day SIV infection as well as 3 uninfected controls. We identified six microglial clusters and two macrophage clusters by transcriptomic profiling. Intriguingly, there were two microglial clusters populated with the cells from infected animals. These two infection-specific clusters had significantly higher expression (p < 0.05) of MHC class I molecules, interferon-induced proteins, chemokines, and cytokines than did the other clusters. Although only a low proportion of SIV-infected cells were detected in microglia and macrophages (~0.14%), almost all the microglia and macrophages in infected animals were activated to certain extents. In addition, the clusters with higher expression of cytotoxic molecules increased their populations during the infection, suggesting their potential to cause HIV-associated neurological disorders.

2024-05-01 | GSE253835 | GEO

RNA sequencing data of microglia, meningeal macrophages (mMΦ) and perivascular macrophages (pvMΦ) isolated from brains of Cx3cr1-GFP mice at different age.

Project description:All tissue resident macrophages of the central nervous system (CNS), including parenchymal microglia as well as CNS-associated macrophages (CAMs) such as meningeal (mMF) and perivascular macrophages (pvMF) are part of the CNS endogenous innate immune system that acts as the first line of defense during infections or trauma. It has been suggested that microglia and all CAM subsets are derived from prenatal cellular sources in the yolk sac that were defined as early erythromyeloid progenitors. However, the precise ontogenetic relationships, the underlying transcriptional programs and the molecular signals that drive the development of distinct CAMs subsets in situ are poorly understood. Using novel fate mapping systems, single-cell profiling and cell-specific mutants, we show that only mMF and microglia share a common prenatal progenitor. In contrast, pvMF originate from perinatal mMF only after birth in an integrin-dependent manner. Furthermore, the establishment of pvMFcritically requires the presence of vascular smooth muscle cells. In summary, our data reveal a novel precisely timed process in distinct anatomical niches for the establishment of CNS macrophage subsets.

2022-01-27 | GSE194432 | GEO

Transcription profiling of monkey model of neuroAIDS reveals induction of pathogenic sets of genes in macrophages and neurons

Project description:The etiology of the central nervous system (CNS) alterations after human immunodeficiency virus (HIV) infection, such as dementia and encephalitis, remains unknown. We have used microarray analysis in a monkey model of neuroAIDS to identify 98 genes, many previously unrecognized in lentiviral CNS pathogenesis, whose expression is significantly up-regulated in the frontal lobe of simian immunodeficiency virus-infected brains. Further, through immunohistochemical illumination, distinct classes of genes were found whose protein products localized to infiltrating macrophages, endothelial cells and resident glia, such as CD163, Glut5, and ISG15. In addition we found proteins induced in cortical neurons (ie, cyclin D3, tissue transglutaminase, 1-antichymotrypsin, and STAT1), which have not previously been described as participating in simian immunodeficiency virus or HIV-related CNS pathology. This molecular phenotyping in the infected brains revealed pathways promoting entry of macrophages into the brain and their subsequent detrimental effects on neurons. These data support the hypothesis that in HIV-induced CNS disease products of activated macrophages and astrocytes lead to CNS dysfunction by directly damaging neurons, as well as by induction of altered gene and protein expression profiles in neurons themselves which are deleterious to their function.

2008-06-12 | E-GEOD-2377 | biostudies-arrayexpress

RNA sequencing data of microglia isolated from brains of WT, Hexb-tdTomato, Hexb-CreERT2 and Hexb-KO mice.

Project description:RNA sequencing data of microglia isolated from brains of WT, Hexb-tdTomato, Hexb-CreERT2 and Hexb-KO mice.

| PRJNA624151 | ENA

Gene expression of macrophages isolated from mouse brains

Project description:Hematogenous macrophages infiltrate the brain after virus infection. We use a CSF1R inhibitior, PLX5622 to deplete microglia from the brain. However, macrophages also express the CSF1R and may be affected by PLX5622-treatment of mice.

2018-02-28 | GSE103379 | GEO

Crosstalk between macrophages and fibro-adipogenic progenitors during muscle regeneration

Project description:The purpose of this study is to investigate how immune cells (macrophages) are closely linked with fibro-adipogenic progenitors (FAPs) during recovery processe. We report that the depletion of Mrc1+ (gene encoding CD206) M2-like macrophages promoted the recovery of muscle after injury. A total RNA sequence analysis of whole muscle or isolated FAPs revealed that the depletion of Mrc1+ M2-like macrophages resulted in the activation of FAPs. Activated FAPs secrete follistatin (Fst), a promyogenic factor, boosting the recovery process. We further determined that the knockdown of FAPs-derived Fst delayed the recovery process. Mechanistically, Mrc1+ M2-like macrophages-specific TGF-b1 inhibited the activation of FAPs, and the FAPs failed to secrete Fst.

2022-09-12 | GSE173555 | GEO

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