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Gene expression profile of MANF-deficient Cx3cr1+ macrophages during muscle regeneration

ABSTRACT: Gene expression profile of MANF-deficient Cx3cr1+ macrophages during muscle regeneration

PROVIDER: PRJNA933219 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23387327_1.fastq.gz	Fastqsanger.gz
	SRR23387327_2.fastq.gz	Fastqsanger.gz
	SRR23387328_1.fastq.gz	Fastqsanger.gz
	SRR23387328_2.fastq.gz	Fastqsanger.gz
	SRR23387329_1.fastq.gz	Fastqsanger.gz

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Gene expression profile of MANF-deficient Cx3cr1+ macrophages during muscle regeneration

Project description:RNA sequencing analysis of MANF-deficient macrophages revealed changes in key cellular processes.

2023-02-13 | GSE224983 | GEO

Investigation of cerebrum proteomic changes in CX3CR1 deficient middle aged mouse

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.

2025-07-05 | PXD058961 | Pride

Immune profiling of DSS-treated Manf-deficient mice by scRNA-seq

Project description:To identify the immune cell populations associated with aggravated colitis in Manf-deficient mice after DSS treatment, we performed scRNA sequencing of CD45+ colonic immune cells

2026-08-20 | GSE337477 | GEO

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.

2019-10-01 | GSE130960 | GEO

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.

2015-09-29 | GSE73473 | GEO

Cx3cr1-deficient microglia exhibit a premature aging transcriptome

2019-11-25 | GSE131869 | GEO

Cx3cr1-deficient microglia exhibit a premature aging transcriptome

Project description:Cx3cr1-deficient microglia exhibit a premature aging transcriptome

| PRJNA542087 | ENA

Cx3cr1-deficient microglia exhibit a premature aging transcriptome

Project description:Cx3cr1-deficient microglia exhibit a premature aging transcriptome

| PRJNA545148 | ENA

Immune profiling of DSS-treated Manf-deficient mice by scRNA-seq

Project description:Immune profiling of DSS-treated Manf-deficient mice by scRNA-seq

| PRJNA1489455 | ENA

Transcriptomic profiling of PBS-treated and MANF-reprogrammed mouse BMDMs

Project description:To investigate whether MANF directly regulates macrophage phenotypes, we treated maturing bone marrow-derived monocytes\macrophages (BMDMs) with MANF or PBS.

2026-08-20 | GSE338361 | GEO

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