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Transcriptional profiles of microglia-like progeny cells derived from Cx3cr1 haplo-insufficient HSPCs and wild-tyoe HSPCs

ABSTRACT: Transcriptional profiles of microglia-like progeny cells derived from Cx3cr1 haplo-insufficient HSPCs and wild-tyoe HSPCs

PROVIDER: PRJNA1170949 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30924102.fastq.gz	Fastqsanger.gz
	SRR30924103.fastq.gz	Fastqsanger.gz
	SRR30924104.fastq.gz	Fastqsanger.gz
	SRR30924105.fastq.gz	Fastqsanger.gz

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Transcriptional profiles of microglia-like progeny cells derived from Cx3cr1 haplo-insufficient HSPCs and wild-tyoe HSPCs

Project description:Favoring the engraftment and maturation of the engineered HSPCs in the central nervous system could allow enhancing further the therapeutic potential of the transplantation of engineered HSPCs for treating neurometabolic diseases. We propose a gene addition strategy involving Cx3cr1, a microglia chemokine receptor regulating microglia ontogeny and function. Here we characterize the transcriptional profile of microglia-like cell generated by Cx3cr1 haplo-insufficient and WT HSPC

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Cx3cr1-deficient microglia exhibit a premature aging transcriptome

Project description:CX3CR1, one of the highest expressed genes in microglia in mice and humans, is implicated in numerous microglial functions. However, the molecular mechanisms underlying Cx3cr1 signaling are not well understood. Here, we analyzed transcriptomes of Cx3cr1-deficient microglia under varying conditions by RNA-Seq. In 2 mos mice, Cx3cr1 deletion resulted in the downregulation of a subset of immune-related genes, without substantial epigenetic changes in markers of active chromatin. Surprisingly, Cx3cr1-deficient microglia from young mice exhibited a transcriptome consistent with that of aged Cx3cr1-sufficient animals, suggesting a premature aging transcriptomic signature. Immunohistochemical analysis of microglia in young and aged mice revealed that loss of Cx3cr1 modulates microglial morphology in a compatible fashion. Our results suggest that CX3CR1 may regulate microglial function in part by modulating the expression levels of a subset of inflammatory genes during chronological aging, making Cx3cr1-deficient mice useful for studying aged microglia.

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Project description:The aging brain shows changes in microglial function, morphology, and phenotype, indicating chronic microglial activation. CX3CR1 is crucial for microglial chemotaxis, phagocytosis, and activation. However, its exact role in the aging brain is not well understood. In this study, we examined the expression of CX3CR1 in the brains of middle-aged mice (10 months old) and explored its functional implications by conducting proteomic profiling in CX3CR1-deficient mouse cerebrum. Proteomic analysis revealed an enrichment of differentially expressed proteins (DE-proteins) in the cerebrum of middle-aged mice in GO pathways such as “synapse”, “translation”, and “ribosome”. CX3CR1 deficiency affected protein levels in GO pathways such as “glutamatergic synapse” and “RNA splicing.” We also detected the proteomics in age-matched 5xFAD mice for comparison, since this mouse strain featured aberrant microglial activation and CX3CR1 upregulation in the hippocampus and frontal cortex. Our findings demonstrated that CX3CR1 was upregulated to maintain synaptic homeostasis probably through regulating microglial activation and phagocytosis in the brains of middle-aged mice. CX3CR1 may represent a promising therapeutic target for alleviating the effects of aging and preventing neurodegeneration.

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Project description:The involvement of microglia in neurodegenerative diseases has drawn increasing attention, as many genetic risk factors are preferentially expressed in microglia. Microglial fractalkine receptor (CX3CR1) signaling regulates many key microglial functions, and the CX3CR1-V249I single nucleotide polymorphism (SNP) has been associated with increased risk for multiple neurodegenerative conditions, including Alzheimer’s disease, yet its functional consequences in human microglia remain unexplored. In this study, we generated iPSC-derived human microglia-like cells (hMGLs) and found that the CX3CR1-V249I variant increased susceptibility to starvation-induced cell death, reduced amyloid-beta uptake, altered microglial morphology, and impaired migration, with more pronounced effects in homozygous cells. Co-culture with neurons demonstrated that hMGLs with the CX3CR1-V249I variant misregulated neuronal properties, including abnormal neuronal growth as well as an induction of neuronal hyperexcitability. These findings highlight the critical role of CX3CR1 in regulating microglial function and implicate the V249I variant in driving pathogenic microglial states relevant to neurodegeneration.

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