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Microglia protect against age-associated brain pathologies

ABSTRACT: Microglia protect against age-associated brain pathologies

PROVIDER: PRJNA1111815 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29039500_1.fastq.gz	Fastqsanger.gz
	SRR29039500_2.fastq.gz	Fastqsanger.gz
	SRR29039501_1.fastq.gz	Fastqsanger.gz
	SRR29039501_2.fastq.gz	Fastqsanger.gz
	SRR29039502_1.fastq.gz	Fastqsanger.gz

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Microglia protect against age-associated brain pathologies

Project description:Microglia are brain-resident macrophages that contribute to central nervous system development, maturation, and preservation. Here, we examine the consequences of lifelong absence of microglia on ageing using the Csf1rΔFIRE/ΔFIRE mouse model. In juvenile Csf1rΔFIRE/ΔFIRE mice, we show that microglia are largely dispensable for the transcriptomic maturation of other brain cell types. In contrast, with advancing age, multiple pathologies accumulate in Csf1rΔFIRE/ΔFIRE brains, astrocytes and oligodendrocyte-lineage cells become increasingly dysregulated, and white matter integrity declines, mimicking many of the pathological features of human CSF1R-related leukoencephalopathy. The thalamus is particularly sensitive to neuropathological changes in the absence of microglia, with atrophy, neuron loss, vascular disturbances, macroglial dysregulation, and severe calcifications all detected in this region. Thalamic calcification formation, which often occurs with normal ageing, is dramatically accelerated in Csf1rΔFIRE/ΔFIRE brains but can be prevented via transplantation of wild-type microglia. Our results indicate that lifelong absence of microglia results in an age-related neurodegenerative condition that can be prevented by the transplantation of healthy microglia.

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Project description:In order to evaluate the gene expression profile of retinal microglia cells in different age, we purified CD11b-positive microglia from the retinas of wild type C57BL/6 mice at 3, 12, 18, and 24 months age using cell sorting method with flow cytometry. Age-related genes from isolated retinal microglia were performed using 16 Affymetrix GeneChips of Mouse Exon 1.0ST Arrays. Gene expression level between consecutive age groups (i.e. between 3 and 12 months, 12 and 18 months, and 18 and 24 months) was examined to identify microglia relevant aging genes that demonstrated significant changes. We identified a total 719 genes that showed increasing or decreasing more than 1.5-fold change (p<0.05, one-way ANOVA) for at least one of the three inter age-group comparisons. These identified genes were subjected to a hierarchical cluster analysis to visualize trends in differential expression across individual biological repeats in the 4 age groups. The microglia cells were isolated from wild type C57BL/6 mice with microglia cell specific marker CD11b conjugated with FITC using flowcytometry sorting. The aging time point was designed as 4 groups: 3 moth, 12 month, 18 month and 24 month; each group includes 4 repeats. The total RNA was extracted from isolated retinal microglia cells and reverse transcripted to cDNA after amplification and labeling. The gene expression profile was detected with Affymetrix GeneChip of Mouse Exon 1.0ST Arrays

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