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Fate mapping via Ms4a3 expression history traces monocyte-derived cells

ABSTRACT: Fate mapping via Ms4a3 expression history traces monocyte-derived cells

PROVIDER: PRJNA555482 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9713850.fastq.gz	Fastqsanger.gz
	SRR9713860.fastq.gz	Fastqsanger.gz
	SRR9713870.fastq.gz	Fastqsanger.gz
	SRR9713880.fastq.gz	Fastqsanger.gz
	SRR9713890.fastq.gz	Fastqsanger.gz

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Fate mapping via Ms4a3 expression history traces monocyte-derived cells

Project description:We performed a single-cell transcriptomic analysis of monocyte and monocyte progenitors by single-cell mRNA sequencing (scRNA-seq) using the C1 Fluidigm platform. We sorted BM cMoPs (Lin−CD117+CD115+CD135−Ly6C+), BM Ly6C+ monocytes (Lin−CD117-CD115+CD135−Ly6C+) and blood Ly6Chi monocytes (CD115+CD11b+Ly6Chi) from wild-type (WT) C57BL/6 mice by fluorescence-activated cell sorting (FACS) and generated transcriptional profiles for each individual cell (n = 38 for blood Ly6Chi monocytes, n = 66 for BM cMoPs, n = 57 for BM Ly6C+ monocytes).

2019-08-19 | GSE134523 | GEO

Notch and TLR signaling coordinate monocyte cell fate and inflammation

Project description:We studied the role of Notch2 signaling in Ly6Chi monocyte cell fate during TLR7-induced acute inflammation. To characterize the gene expression changes involved in monocyte differentiation, we subjected monocyte subsets from peripheral blood of wt and myeloid Notch2 mutant mice after Sham or IMQ treatment to RNA-sequencing and gene expression analysis. We found that Cell-intrinsic Notch2 and TLR7-Myd88 pathways independently and synergistically promote Ly6Clo patrolling monocyte development from Ly6Chi monocytes under inflammatory conditions. At the same time TLR7 stimulation in the absence of functional Notch2 signaling promotes resident tissue macrophage gene expression signatures in monocytes and ectopic differentiation of Ly6Chi monocytes into macrophages and dendritic cells. Thus, Notch2 is a master regulator of Ly6Chi monocyte cell fate and inflammation in response to TLR signaling.

2020-08-04 | GSE147492 | GEO

Fate-mapping via Spp1-expression history revealed innate immune memory of microglia imprinted by neonatal injury

Project description:Fate-mapping via Spp1-expression history revealed innate immune memory of microglia imprinted by neonatal injury

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Fate-mapping via Spp1-expression history revealed innate immune memory of microglia imprinted by neonatal injury [Spp1Tdt]

Project description:Microglial reactivity to injury and disease is emerging as a heterogeneous, dynamic, and crucial determinant in neurological disorders. However, the plasticity and ultimate fate of disease-associated microglia (DAM) remains largely unknown. We established a lineage tracing system, leveraging the expression dynamics of Spp1, which allows for genetic labeling of DAM-like microglia and tracking their behavior during brain injury and recovery. Fate-mapping of Spp1+ microglia in juvenile stroke revealed an irreversible state of reactive microglia that are ultimately eliminated from the injured brain. In contrast, DAM-like microglia in the neonatal context exhibit high plasticity, capable of regaining a homeostatic signature and integrating into the global microglial network after recovery. Furthermore, neonatal injury has a lasting impact on microglia, rendering them intrinsically sensitized to subsequent immune challenges. Therefore, by unraveling the fate of DAM-like microglia in various neuropathological conditions, our work highlights the exceptional plasticity and innate immune memory of neonatal microglia.

2024-01-24 | GSE247391 | GEO

Fate-mapping via Spp1-expression history revealed innate immune memory of microglia imprinted by neonatal injury [Spp1GFP]

2024-01-24 | GSE247390 | GEO

Fate-mapping via Spp1-expression history revealed innate immune memory of microglia imprinted by neonatal injury [Spp1GFP]

Project description:Fate-mapping via Spp1-expression history revealed innate immune memory of microglia imprinted by neonatal injury [Spp1GFP]

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Fate-mapping via Spp1-expression history revealed innate immune memory of microglia imprinted by neonatal injury [Spp1Tdt]

Project description:Fate-mapping via Spp1-expression history revealed innate immune memory of microglia imprinted by neonatal injury [Spp1Tdt]

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Zeb2 regulates commitment to plasmacytoid dendritic cell and monocyte fate

Project description:Zeb2 regulates commitment to plasmacytoid dendritic cell and monocyte fate

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Notch and TLR signaling coordinate monocyte cell fate and inflammation

Project description:Notch and TLR signaling coordinate monocyte cell fate and inflammation

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Fate mapping via CCR2-CreER mice reveals monocyte-to-microglia transition in development and neonatal stroke.

Project description:Whether monocytes contribute to the brain microglial pool in development or after brain injury remains contentious. To address this issue, we generated CCR2-CreER mice to track monocyte derivatives in a tamoxifen-inducible manner. This method labeled Ly6Chi and Ly6Clo monocytes after tamoxifen dosing and detected a surge of perivascular macrophages before blood-brain barrier breakdown in adult stroke. When dosed by tamoxifen at embryonic day 17 (E17), this method captured fetal hematopoietic cells at E18, subdural Ki67+ ameboid cells at postnatal day 2 (P2), and perivascular microglia, leptomeningeal macrophages, and Iba1+Tmem119+P2RY12+ parenchymal microglia in selective brain regions at P24. Furthermore, this fate mapping strategy revealed an acute influx of monocytes after neonatal stroke, which gradually transformed into a ramified morphology and expressed microglial marker genes (Sall1, Tmem119, and P2RY12) for at least 62 days after injury. These results suggest an underappreciated level of monocyte-to-microglia transition in development and after neonatal stroke.

| S-EPMC7449686 | biostudies-literature

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