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Tissue resident macrophages promote renal cystic disease

ABSTRACT: Tissue resident macrophages promote renal cystic disease

PROVIDER: PRJNA545273 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9141590_1.fastq.gz	Fastqsanger.gz
	SRR9141590_2.fastq.gz	Fastqsanger.gz
	SRR9141591_1.fastq.gz	Fastqsanger.gz
	SRR9141591_2.fastq.gz	Fastqsanger.gz

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Tissue resident macrophages promote renal cystic disease

Project description:We show that resident macrophages accumulate in cilia mutant mice prior to cyst formation and that inhibition of resident macrophage accumulation reduces cystic kidney disease.

2019-07-04 | GSE131896 | GEO

Identification of renal resident macrophages across species

Project description:Identification of renal resident macrophages across species

| PRJNA529654 | ENA

Tissue-Resident Macrophages Promote Renal Cystic Disease.

Project description:BackgroundMutations affecting cilia proteins have an established role in renal cyst formation. In mice, the rate of cystogenesis is influenced by the age at which cilia dysfunction occurs and whether the kidney has been injured. Disruption of cilia function before postnatal day 12-14 results in rapid cyst formation; however, cyst formation is slower when cilia dysfunction is induced after postnatal day 14. Rapid cyst formation can also be induced in conditional adult cilia mutant mice by introducing renal injury. Previous studies indicate that macrophages are involved in cyst formation, however the specific role and type of macrophages responsible has not been clarified.MethodsWe analyzed resident macrophage number and subtypes during postnatal renal maturation and after renal injury in control and conditional Ift88 cilia mutant mice. We also used a pharmacological inhibitor of resident macrophage proliferation and accumulation to determine the importance of these cells during rapid cyst formation.ResultsOur data show that renal resident macrophages undergo a phenotypic switch from R2b (CD11clo) to R2a (CD11chi) during postnatal renal maturation. The timing of this switch correlates with the period in which cyst formation transitions from rapid to slow following induction of cilia dysfunction. Renal injury induces the reaccumulation of juvenile-like R2b resident macrophages in cilia mutant mice and restores rapid cystogenesis. Loss of primary cilia in injured conditional Ift88 mice results in enhanced epithelial production of membrane-bound CSF1, a cytokine that promotes resident macrophage proliferation. Inhibiting CSF1/CSF1-receptor signaling with a CSF1R kinase inhibitor reduces resident macrophage proliferation, R2b resident macrophage accumulation, and renal cyst formation in two mouse models of cystic disease.ConclusionsThese data uncover an important pathogenic role for resident macrophages during rapid cyst progression.

| S-EPMC6779366 | biostudies-literature

Identification of renal resident macrophages across species [10X]

Project description:Identification of renal resident macrophages across species [10X]

| PRJNA529656 | ENA

Identification of renal resident macrophages across species [C1]

Project description:Identification of renal resident macrophages across species [C1]

| PRJNA529657 | ENA

Gene signature of mouse skin resident macrophages

Project description:Skin resident macrophages were isolated by FACS sorting at different ages post natally and RNA was extracted mouse skin resident macrophages

2014-05-30 | E-GEOD-58098 | biostudies-arrayexpress

Identification of renal resident macrophages across species [10X]

Project description:We use single cell RNA sequencing to identify an evolutionarily conserved gene expression signature in resident macrophages. Based on our single cell data, we show the presence of a core gene expression signature in a cluster of innate immune cells in mouse, rat, pig, and human kidney tissue. Further, using this gene expression signature, we identify novel candidate markers for resident macrophages that span all 4 species tested.

2019-04-05 | GSE128992 | GEO

Identification of renal resident macrophages across species [C1]

2019-04-05 | GSE128991 | GEO

Gene expression in inflammatory macrophages, tissue resident macrophages and neutrophils

Project description:Genes expression in Ly6C+/F4/80+ inflammatory macrophages, CX3CR1+/F4/80+ tissue resident macrophages and Ly6G+/F4/80- neutrophils which were isolated from day 3 wounds in C57/B6 mice aged 8 weeks by cell sorting Ly6C+ macrophages expressed higher (over 5 folds) levels of 241 genes compared to CX3CR1+ macrophages, and 3382 genes compared to neutrophils

2016-07-01 | E-GEOD-74783 | biostudies-arrayexpress

Self-renewing resident cardiac macrophages limit adverse remodeling following myocardial infarction

Project description:Mononuclear phagocytes promote injury and repair following myocardial infarction but discriminating functions within mixed populations remains challenging. We utilized fate mapping and single cell RNA-sequencing to delineate fate specification trajectories of heterogeneous cardiac macrophage subpopulations. In steady state, TIMD4 expression tracked with a dominant resident cardiac macrophage subset that persisted via in situ self-renewal with minimal monocyte input. Following ischemic injury, monocytes displayed significant plasticity, ultimately adopting transcriptional states similar to resident macrophages, but also multiple unique states. Ischemic injury reduced resident macrophage abundance within infarct tissue, and despite transcriptional similarity, TIMD4 expression distinguished resident from recruited macrophages. Specific lineage-based depletion of resident cardiac macrophages resulted in depressed cardiac function and adverse remodeling primarily within the peri-infarct zone, the only region of the myocardium where resident macrophages expanded numerically following injury. Together, these data highlight a non-redundant, cardioprotective role of resident cardiac macrophages, and the diverse transcriptional fates recruited monocytes can adopt.

2018-12-15 | GSE119355 | GEO

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