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Gene expression profile at single cell level of peripheral blood mononuclear cells from Cx3cr1-/- mice and wt mice under C57BL/6J background

ABSTRACT: Gene expression profile at single cell level of peripheral blood mononuclear cells from Cx3cr1-/- mice and wt mice under C57BL/6J background

PROVIDER: PRJNA1189150 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31438611_1.fastq.gz	Fastqsanger.gz
	SRR31438611_2.fastq.gz	Fastqsanger.gz
	SRR31438612_1.fastq.gz	Fastqsanger.gz
	SRR31438612_2.fastq.gz	Fastqsanger.gz
	SRR31438613_1.fastq.gz	Fastqsanger.gz

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Gene expression profile at single cell level of peripheral blood mononuclear cells from Cx3cr1-/- mice and wt mice under C57BL/6J background

Project description:CX3CR1 is a receptor for chemokines, primarily expressed in peripheral blood mononuclear cells, particularly in monocytes and macrophages. It influences the chemotaxis, adhesion, and migration of immune cells to vascular endothelial cells. We used peripheral blood from Cx3cr1 monocyte/macrophage-specific knockout mice for single-cell sequencing to analyze the changes in monocytes, macrophages, and other cells in the circulating blood after knockout.

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Mononuclear phagocytes in muscle after notexin injury in C57Bl/6, Cx3cr1-/-, Ccl2-/-,Cx3cr1-/-Ccl2-/- mice

Project description:Muscle injury triggers inflammation in which infiltrating mononuclear phagocytes are crucial for tissue regeneration. The interaction of the CCL2/CCR2 and CX3CL1/CX3CR1 chemokine axis that guides phagocyte infiltration is incompletely understood. Here, we show that CX3CR1 deficiency promotes muscle repair and rescues Ccl2-/- mice from impaired muscle regeneration as a result of altered macrophage function, not infiltration. Transcriptomic analysis of muscle mononuclear phagocytes reveals that Apolipoprotein E (ApoE) is up-regulated in mice with efficient regeneration. ApoE treatment enhances phagocytosis by mononuclear phagocytes in vitro, and restores phagocytic activity and muscle regeneration in Ccl2-/- mice. Because CX3CR1 deficiency may compensate for defective CCL2-dependant monocyte recruitment by modulating ApoE-dependent macrophage phagocytic activity, targeting CX3CR1 expressed by macrophages might be a powerful therapeutic approach to improve muscle regeneration.

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Project description:Add1 Null mice on the C57BL/6J background develop hydrocephalus that may be due to gene expression changes in the choroid plexus. We used microarrays to detail choroid plexi gene expression prior to the manifestation of hydrocephalus. Choroid plexi from the four ventricle were dissected out, for RNA extraction and hybridization to Affymetrix microarrays, from male Add1 wildtype, heterozygous and null mice at three weeks of age. Five mice were selected for each genotype to assess gene expression prior to the development of hydrocephalus.

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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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