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Microglia response upon demyelinating injury [ATAC-seq]

ABSTRACT: Microglia response upon demyelinating injury [ATAC-seq]

PROVIDER: PRJNA957805 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24230453_1.fastq.gz	Fastqsanger.gz
	SRR24230453_2.fastq.gz	Fastqsanger.gz
	SRR24230454_1.fastq.gz	Fastqsanger.gz
	SRR24230454_2.fastq.gz	Fastqsanger.gz
	SRR24230455_1.fastq.gz	Fastqsanger.gz

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Microglia response upon demyelinating injury [snRNA-seq]

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Microglia response upon demyelinating injury [ATAC-seq]

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Microglia response upon demyelinating injury [snRNA-seq]

Project description:Following demyelinating injury, aged mice have poor recovery compared to young mice. We perforned snRNA seq on the white matter isolated from young and old mice after lesion induction to characterize the transcriptomic signature of glial cells with particular focus on microglia.

2024-07-24 | GSE230480 | GEO

Mitochondrial respiration in microglia is essential for response to demyelinating injury but not proliferation

Project description:Microglia are necessary for CNS function during development and play roles in aging, Alzheimer’s Disease (AD) and the response to demyelinating injury. Mitochondrial respiratory chain (RC) is necessary for conventional T cell proliferation6 and macrophage-dependent immune responses. However, whether mitochondrial RC is essential for microglia proliferation or function is not known. We conditionally deleted the mitochondrial complex III subunit Rieske Iron-Sulfur Protein (RISP) in the microglia of adult mice to assess the requirement of microglial RC for survival, proliferation, and adult CNS function in vivo. Surprisingly, mitochondrial RC function was not required for survival or proliferation of microglia in vivo. RNA-seq analysis showed that loss of RC function in microglia caused changes in gene expression distinct from aged or disease-associated microglia (DAM). Microglia-specific loss of mitochondrial RC function is not sufficient to induce cognitive decline. Amyloid-β plaque coverage decreased and microglial interaction with Amyloid-β plaques increased in the hippocampus of 5xFAD mice with mitochondrial RC-deficient microglia. Microglia-specific loss of mitochondrial RC function did impair remyelination following an acute, reversible demyelinating event. Thus, mitochondrial respiration in microglia is dispensable for proliferation but is essential to maintain a proper response to CNS demyelinating injury.

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Effect of trained immune response upon demyelinating injury in brain [RNA-seq]

Project description:Effect of trained immune response upon demyelinating injury in brain [RNA-seq]

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Mitochondrial respiration in microglia is essential for response to demyelinating injury but not proliferation

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Aging-exacerbated demyelinating injury is associated with microglia-derived reactive oxygen species: alleviation by indapamide

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Pro-inflammatory activity following demyelinating injury is required for phagocytic function and oligodendrocyte formation

Project description:Remyelination can occur naturally in demyelinating lesions, but often fails in human demyelinating diseases such as multiple sclerosis (MS). The function of the innate immune system is essential for the regenerative response, but how exactly microglia and macrophages clear myelin debris after injury and tailor a specific regenerative response is unclear. Here, we asked whether pro-inflammatory microglial/macrophage activation is required for this process. We established a novel toxin-based spinal cord model of de- and remyelination in zebrafish and showed that pro-inflammatory nuclear factor κB (NF-κB) dependent activation occurs in phagocytes rapidly after myelin injury. We found that the pro-inflammatory response depends on myeloid differentiation primary response 88 (MyD88), the canonical adaptor for inflammatory signaling pathways downstream of toll-like receptors (TLRs). MyD88-deficient mice and zebrafish were impaired not only in the degradation of myelin debris, but also in initiating the generation of new oligodendrocytes for myelin repair. We identified reduced generation of tumor necrosis factor-α (TNF-α) in lesions of MyD88-deficient animals, a pro-inflammatory molecule that was able to induce the generation of new oligodendrocytes. Our study shows that pro-inflammatory phagocytic signaling is an evolutionary conserved mechanism necessary for degrading myelin debris, essential for inflammation resolution, and for initiating the secretion of pro-inflammatory myelin repair molecules.

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