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