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Human iPSC-derived microglia assume a primary microglia-like state after transplantation into the neonatal mouse brain [Single Cell RNAseq]

ABSTRACT: iPSC derived microglial precursors were tranplanted into the brains of neonatal mice, FACS sorted out based on GFP+ following 2 months, and compared to in vitro differentiated iPSC derived microglia from the same precursors.

ORGANISM(S): Homo sapiens

PROVIDER: GSE139193 | GEO | 2019/11/27

REPOSITORIES: GEO

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Human iPSC-derived microglia assume a primary microglia-like state after transplantation into the neonatal mouse brain [Bulk RNAseq]

Project description:iPSC derived microglial precursors were transplanted into the brains of neonatal mice, FACS sorted out based on GFP+ following 2 months, and compared to in vitro differentiated iPSC derived microglia from the same precursors.

2019-11-27 | GSE139192 | GEO

Functional Mature Human Microglia Developed in Human iPSC Microglial Chimeric Mouse Brain

Project description:Microglia, the brain-resident macrophages, exhibit highly dynamic functions in neurodevelopment and neurodegeneration. Human microglia possess unique features as compared to mouse microglia, but our understanding of human microglial functions is largely limited by an inability to obtain human microglia under homeostatic states. We developed a human pluripotent stem cell (hPSC)-based microglial chimeric mouse brain model by transplanting hPSC-derived primitive macrophage precursors into neonatal mouse brains. The engrafted human microglia widely disperse in the brain and replace mouse microglia in corpus callosum at 6 months post-transplantation. Single-cell RNA-sequencing of the microglial chimeric mouse brains reveals that xenografted hPSC-derived microglia largely retain human microglial identity, as they exhibit signature gene expression patterns consistent with physiological human microglia and recapitulate heterogeneity of adult human microglia. Importantly, the engrafted hPSC-derived microglia exhibit dynamic response to cuprizone-induced demyelination and species-specific transcriptomic differences in the expression of neurological disease-risk genes in microglia. This model will serve as a novel tool to study the role of human microglia in brain development and degeneration.

2020-02-22 | GSE139161 | GEO

Gene expression from neonatal human fibroblasts and MV-derived iPSC clones

Project description:Measles virus vector expressing the 4 reprogramming factors, OCT4, SOX2, KLF4 and cMYC was produced and used to derived iPSC from neonatal human fibroblasts (BJ). We used microarrays to compare the global gene expression in the derived MV-iPSC and compare it to the parental human neonatal fibroblast (BJ) and human embryonic stem cell (GSM551202)

2019-09-26 | GSE122790 | GEO

Xenotransplantation of Human PSC-derived Microglia Creates a Chimeric Mouse Brain Model that Recapitulates Features of Adult Human Microglia

Project description:Microglia, the brain-resident macrophages, exhibit highly dynamic functions in neurodevelopment and neurodegeneration. Human microglia possess unique features as compared to mouse microglia, but our understanding of human microglial functions is largely limited by an inability to obtain human microglia under resting, homeostatic states. We developed a human pluripotent stem cell (hPSC)-based microglial chimeric mouse brain model by transplanting hPSC-derived primitive macrophage precursors into neonatal mouse brains. The engrafted human microglia widely disperse in the brain and replace mouse microglia in corpus callosum at 6 months post-transplantation. Single-cell RNA-sequencing of the hPSC microglial chimeric mouse brains reveals that xenografted hPSC-derived microglia largely retain human microglial identity, as they exhibit signature gene expression patterns consistent with physiological human microglia and recapitulate heterogeneity of adult human microglia. Importantly, the chimeric mouse brain also models species-specific transcriptomic differences in the expression of neurological disease-risk genes in microglia. This model will serve as a novel tool to study the role of human microglia in brain development and degeneration.

2019-04-02 | GSE129178 | GEO

Human iPSC-derived microglia assume a primary microglia-like state after transplantation into the neonatal mouse brain

Project description:Human iPSC-derived microglia assume a primary microglia-like state after transplantation into the neonatal mouse brain

| PRJNA578719 | ENA

Location of Neonatal Microglia Drives Small Extracellular Vesicles Content and Biological Functions

Project description:Combining proteomics and systems biology analyses, we demonstrated that neonatal microglial cells derived from two different CNS locations (cortex and spinal cord) displayed different phenotypes upon different physiological or pathological conditions. These cells also exhibited great variability in terms of both cellular and small extracellular vesicles (sEVs) protein contents and levels. Bioinformatics data analysis showed that the cortical microglia had anti-inflammatory and neurogenesis/tumorigenesis properties, while the spinal cord microglia was rather involved in inflammatory response process. Of interest, while both sEVs microglia sources enhanced growth of DRGs axons, only the spinal cord-derived sEVs microglia under LPS stimulation significantly attenuated glioma proliferation. These results were confirmed through neurite outgrowth assays in DRGs cell line and glioma proliferation analysis in 3D spheroid cultures. Results from these in vitro assays indicated that the microglia localized at different CNS regions can ensure different biological functions. Together, these works indicate that neonatal microglia locations regulate their physiological and pathological functional fates, and could explain the high prevalence of brain vs. spinal cord glioma in adults.

2020-05-26 | PXD016093 | Pride

Human iPSC-derived microglia assume a primary microglia-like state after transplantation into the neonatal mouse brain [Bulk RNAseq]

Project description:Human iPSC-derived microglia assume a primary microglia-like state after transplantation into the neonatal mouse brain [Bulk RNAseq]

| PRJNA578732 | ENA

Human iPSC-derived microglia assume a primary microglia-like state after transplantation into the neonatal mouse brain [Single Cell RNAseq]

Project description:Human iPSC-derived microglia assume a primary microglia-like state after transplantation into the neonatal mouse brain [Single Cell RNAseq]

| PRJNA578733 | ENA

Transcription profiling of neonatal rat microglia after IFN-gamma activation

Project description:IFN-gamma is a classical microglial stimulant. We used microarrays to investigate the microglial gene regulatory network activated by interferon-gamma. Experiment Overall Design: Primary rat microglia cultures were established and maintained for 15 days. For activation studies, fresh media containing IFN-gamma (100 U/ml) were added and left overnight (16 hours). Total RNA was extraction and hybridized on Affymetrix microarrays (RG_U34A). Five arrays were run from total RNA derived from unstimulated 5 independent cultures (Mgl_CON1, Mgl_CON2, Mgl_CON3, Mgl_CON5 and Mgl_CON6). Three standard microglial cultures were stimulated (Mgl_IFNgamma_2 and Mgl_IFNgamma_3) with one of the samples analysed in triplicate as a technical control (Mgl_IFNgamma_1a, Mgl_IFNgamma_1b and Mgl_IFNgamma_1c).

2008-06-14 | E-GEOD-6353 | biostudies-arrayexpress

iPSC-derived microglia carrying the TREM2 R47H/+ mutation are pro-inflammatory and promote synapse loss.

Project description:Genetic findings have highlighted key roles for microglia in the pathology of neurodegenerative conditions such as Alzheimer’s disease (AD). A number of mutations in the microglial protein TREM2 (triggering receptor expressed on myeloid cells 2) have been associated with increased risk for developing Alzheimer’s disease (AD), most notably the R47H/+ substitution. We employed gene editing and stem cell models to gain insight into the effects of the TREM2 R47H/+ mutation on human iPSC-derived microglia. We found transcriptional changes affecting numerous cellular processes, with R47H/+ cells exhibiting a pro-inflammatory gene expression signature. TREM2 R47H/+ also caused impairments in microglial movement and the uptake of multiple substrates, as well as rendering microglia hyper-responsive to inflammatory stimuli. We developed an in vitro laser-induced injury model in neuron-microglia co-cultures, finding an impaired injury response by TREM2 R47H/+ microglia. Furthermore, mouse brains transplanted with TREM2 R47H/+ microglia exhibited reduced synaptic density, with upregulation of multiple complement cascade components in TREM2 R47H/+ microglia suggesting inappropriate synaptic pruning as one potential mechanism. These findings identify a number of potentially detrimental effects of the TREM2 R47H/+ mutation on microglial gene expression and function likely to underlie its association with AD.

2024-03-06 | GSE241858 | GEO

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