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A Cre-deleter specific for embryo-derived brain macrophages reveals distinct features of microglia and border macrophages

ABSTRACT: A Cre-deleter specific for embryo-derived brain macrophages reveals distinct features of microglia and border macrophages

PROVIDER: PRJNA878792 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21508200.fastq.gz	Fastqsanger.gz
	SRR21508201_1.fastq.gz	Fastqsanger.gz
	SRR21508201_2.fastq.gz	Fastqsanger.gz
	SRR21508202.fastq.gz	Fastqsanger.gz
	SRR21508203_1.fastq.gz	Fastqsanger.gz

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A Cre-deleter specific for embryo-derived brain macrophages reveals distinct features of microglia and border macrophages

Project description:Genetic tools to target microglia specifically and efficiently from the early stages of the embryonic development are missing. Here we present Crybb1-Cre, a new constitutive Cre deleter producing a nearly complete recombination of embryonic brain macrophages (microglia and embryonic BAMs) by the perinatal period, with limited recombination leakage in peripheral myeloid cells. Using this tool, in combination with Flt3-Cre lineage tracer, scRNA-seq analysis and confocal imaging we were able to accurately fate-map embryonic derived versus monocyte derived BAMs in the mouse cortex and identified specific surface markers to resolve either population. Furthermore, we used Crybb1-Cre to delete the transcription factor SMAD4. Using multiomics analysis combining single-cell RNA-seq and ATAC-seq we showed that SMAD4-deficient microglia underwent an arrest of their homeostatic maturation and at the same time acquired a BAMs specification signature. By contrast, BAMs development was unaffected. Therefore, SMAD4 drives a transcriptional and epigenetic program that is indispensable for the commitment of brain macrophages to the microglia fate. This data provides a valuable resource to study molecular underpinnings of microglia development.

2023-02-02 | GSE213020 | GEO

Parenchymal border macrophages regulate CSF flow dynamics

Project description:Parenchymal border macrophages regulate CSF flow dynamics

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Oligodendrocyte progenitor cells and macrophages/microglia produce glioma stem cell niche at the tumor border

Project description:Characterization of the tumor border microenvironment is critical for improving prognosis in patients with GBM. Here, we compared microRNA (miRNA) expression in samples from the tumor, tumor border, and peripheral region far from tumor mass by miRNA microarray. The top three of miRNAs showing higher expression in the tumor border were related to oligodendrocyte differentiation, and pathologically oligodendrocyte lineage cells were increased in the border, where numbers of macrophages and microglia also colocalized. Medium cultured with oligodendrocyte progenitor cells (OPCs) and macrophages induced stemness and chemo-radioresistance in GBM cells. Thus, OPCs and macrophages/microglia may form a glioma stem cell niche at the tumor border, representing a novel promising target for prevention of recurrence.

2018-01-26 | GSE109628 | GEO

Border-associated macrophages mediate the neuroinflammatory response in an alpha-synuclein model of Parkinson disease

Project description:Neuroinflammation and accumulation of alphα-synuclein (α-syn) are core features of Parkinson disease (PD). We found that α-syn-induced neuroinflammation is driven by antigen presentation from CNS resident macrophages. A subset of these, border-associated macrophages (BAMs), expand and express genes and proteins necessary for immune cell recruitment, infiltration, and antigen presentation, whereas depletion of BAMs prevents neuroinflammation and neurodegeneration. These results point to a critical role for BAMs in initiating PD pathogenesis.

2021-06-20 | GSE178498 | GEO

Parenchymal border macrophages regulate CSF flow dynamics [5xFAD]

Project description:Parenchymal border macrophages regulate CSF flow dynamics [5xFAD]

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Parenchymal border macrophages regulate CSF flow dynamics [brain]

Project description:Parenchymal border macrophages regulate CSF flow dynamics [brain]

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Mouse Embryo Sox1 cre-dependent knockout of EED

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Parenchymal border macrophages regulate CSF flow dynamics [leptomeningeal macs]

Project description:Parenchymal border macrophages regulate CSF flow dynamics [leptomeningeal macs]

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Parenchymal border macrophages regulate CSF flow dynamics [CLO depletion]

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Border-zone cardiomyocytes and macrophages contribute to remodeling of the extracellular matrix to promote cardiomyocyte invasion during zebrafish cardiac regeneration

Project description:Despite numerous advances in our understanding of zebrafish cardiac regeneration, an aspect that remains less studied is how newly proliferated cardiomyocytes invade, and eventually replace, the collagen-containing fibrotic tissue following injury. Here, we provide an in-depth analysis of the process of cardiomyocyte invasion and migration using live-imaging and histological approaches. We observed a close interaction between protruding cardiomyocytes and macrophages at the wound border zone, and irf8 mutant zebrafish, which largely lack macrophages, exhibited defects in extracellular matrix (ECM) remodeling and cardiomyocyte protrusion into the injured area. Using a resident macrophage ablation model, we show that defects in ECM remodeling at the border zone and subsequent cardiomyocyte protrusion can be partly attributed to a population of resident macrophages. Single-cell RNA-sequencing analysis of cells at the wound border revealed a population of cardiomyocytes and macrophages with fibroblast-like gene expression signatures, including the expression of genes encoding ECM structural proteins and ECM-remodeling proteins. The expression of mmp14b, which encodes a membrane-anchored matrix metalloproteinase, was restricted to cells in the border zone and genetic deletion of mmp14b led to a decrease in 1) collagen degradation at the border zone, 2) macrophage recruitment to the border zone, and 3) subsequent cardiomyocyte invasion. Furthermore, cardiomyocyte-specific overexpression of mmp14b was sufficient to enhance cardiomyocyte invasion both into the injured area and along the apical surface of the wound. Altogether, our data shed important insights into the process of cardiomyocyte invasion of the collagen-containing injured tissue during cardiac regeneration. They further suggest that cardiomyocytes and resident macrophages contribute to ECM remodeling at the border zone to promote cardiomyocyte replenishment of the fibrotic injured tissue.

2025-03-11 | GSE251856 | GEO

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