Similar Datasets
Project description:single cell gene expression profiling of microglia after peripheral nerve injury in Cx3cr1-yfp-creER/+ animals and Cx3cr1-yfp-creER/+; Tnfaip3 fl/fl animals
2022-04-19 | GSE163948 | GEO
Project description:Self-renewal of Differentiated Microglia Involves Two Distinct Mechanisms
| PRJNA596938 | ENA
Project description:Self-renewal of Differentiated Microglia Involves Two Distinct Mechanisms II
| PRJNA688303 | ENA
Project description:During early embryogenesis microglia arise from yolk sac progenitors populating the developing CNS, where they are maintained as tissue-resident macrophages throughout the organism’s lifespan. Here, we describe an experimental system that allows the specific conditional ablation of microglia in vivo. Strikingly, we found that the microglia compartment was reconstituted within one week following depletion. Microglia repopulation relied entirely on a CNS-resident, internal pool and was independent from bone marrow-derived precursors. Newly formed microglia were found in highly proliferative, organized micro-clusters that dissolve once steady state was achieved. Gene expression profiling revealed prominent expression of Interleukin-1 (IL-1) receptor in proliferating microglia. During the repopulation phase, IL-1 signaling was neutralized by treatment with IL-1 receptor antagonist that impaired microglia proliferation. Hence, microglia harbor a highly efficient potential to restore themselves without contribution of peripheral myeloid cells. IL-1 signaling significantly participates in this restorative proliferation process and is involved in stabilizing microglia maintenance. bone marrow macrophages, wild type microglia, and repopulating microglia
2015-07-15 | E-GEOD-68376 | biostudies-arrayexpress
Project description:Microglia in the spinal dorsal horn have been implicated in the pathogenesis of neuropathic pain following peripheral nerve injury. We have revently found that CD11c-expressing spinal microglia appear after the development of behavioral pain hypersensitivity following nerve injury and are essential for recovery from neuropathic pain. In order to better understand the gene expression profiles of CD11c-expressing microglia, we performed quantitative bulk RNA sequencing of microglia isolated from mice expressing Venus fluorescent protein under the control of CD11c promoter. We found that CD11c-expressing microglia show distinct gene expression profile compared to CD11c-negative microglia following nerve injury.
2022-04-18 | GSE200856 | GEO
Project description:Microglia constitute a highly specialized network of tissue resident immune cells that is important for the control of tissue homeostasis and the resolution of virtually all diseases of the central nervous system (CNS). However, how this dissemination is established and maintained in vivo and its kinetics of these processes are poorly understood. Here we established a new multicolor fluorescence fate mapping system to monitor microglia dynamics during steady state and disease. Our findings that microglia establish a stable network over time albeit with regional differences and remarkably high turnover rates challenge their postulated longevity. Microglia self-renewal constitutes a random process without evidence of defined progenitor cells. Under pathological conditions this randomness shifts to clonal microglia expansion that is finally resolved by both cell apoptosis and egression for re-establishment of the stable microglia network. Our data reveal new insights on how microglia ensure their complex distribution throughout the healthy and diseased CNS .
2017-03-27 | GSE79252 | GEO
Project description:Hoxb8 mutant mice show compulsive behavior similar to trichotillomania, a human obsessive-compulsive-spectrum disorder. The only Hoxb8 lineage-labeled cells in the brains of mice are microglia, suggesting that defective Hoxb8 microglia caused the disorder. What is the source of the Hoxb8 microglia? It has been posited that all microglia progenitors arise at embryonic day (E) 7.5 during yolk sac hematopoiesis, and colonize the brain at E9.5. In contrast, we show the presence of two microglia subpopulations: canonical, non-Hoxb8 microglia and Hoxb8 microglia. Unlike non- Hoxb8 microglia, Hoxb8 microglia progenitors appear to be generated during the second wave of yolk sac hematopoiesis, then detected in the aorto-gonad-mesonephros (AGM) and fetal liver, where they are greatly expanded, prior to infiltrating the E12.5 brain. Further, we demonstrate that Hoxb8 hematopoietic progenitor cells taken from fetal liver are competent to give rise to microglia in vivo. Although the two microglial subpopulations are very similar molecularly, and in their response to brain injury and participation in synaptic pruning, they show distinct brain distributions which might contribute to pathological specificity. Non-Hoxb8 microglia significantly outnumber Hoxb8 microglia, but they cannot compensate for the loss of Hoxb8 function in Hoxb8 microglia, suggesting further crucial differences between the two subpopulations.
2019-01-07 | GSE124710 | GEO
Project description:During early embryogenesis microglia arise from yolk sac progenitors populating the developing CNS, where they are maintained as tissue-resident macrophages throughout the organism’s lifespan. Here, we describe an experimental system that allows the specific conditional ablation of microglia in vivo. Strikingly, we found that the microglia compartment was reconstituted within one week following depletion. Microglia repopulation relied entirely on a CNS-resident, internal pool and was independent from bone marrow-derived precursors. Newly formed microglia were found in highly proliferative, organized micro-clusters that dissolve once steady state was achieved. Gene expression profiling revealed prominent expression of Interleukin-1 (IL-1) receptor in proliferating microglia. During the repopulation phase, IL-1 signaling was neutralized by treatment with IL-1 receptor antagonist that impaired microglia proliferation. Hence, microglia harbor a highly efficient potential to restore themselves without contribution of peripheral myeloid cells. IL-1 signaling significantly participates in this restorative proliferation process and is involved in stabilizing microglia maintenance.
2015-07-15 | GSE68376 | GEO
Project description:Spinal microglia play a pivotal role in the development of neuropathic pain. Peripheral nerve injury induces changes in the transcriptional profile of microglia, including increased expression of components of translational machinery. Whether microglial protein synthesis is stimulated following nerve injury and has a functional role in mediating pain hypersensitivity is unknown. Here, we show that nascent protein synthesis is upregulated in spinal microglia following peripheral nerve injury. Stimulating mRNA translation in microglia, via selective ablation of the translational repressor, eukaryotic initiation factor 4E-binding protein 1 (4E-BP1), promoted the transition of microglia to a reactive state and induced mechanical hypersensitivity. Conversely, inhibiting microglial translation by expressing mutant 4E-BP1 in microglia attenuated their peripheral nerve injury-induced activation and alleviated neuropathic pain. Thus, the stimulation of 4E-BP1-dependent translation promotes microglia reactivity and mechanical hypersensitivity, whereas its inhibition alleviates neuropathic pain.
2024-01-31 | GSE254472 | GEO
Project description:To examine the effect of Nf1 inactivation in astrocytes on normal microglia in the optic nerve, microglia from Nf1 flox/flox (FF) and Nf1 flox/flox; GFAP-Cre (FFC) were flow sorted. High throughput RNA-seq was employed to compare the expression profiles, and upregulated genes in microglia supportive to Nf1 deficient astrocytes were verified.
2020-07-03 | GSE65865 | GEO