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Resident Macrophages Reprogram Toward a Developmental State After Acute Kidney Injury

ABSTRACT: Resident Macrophages Reprogram Toward a Developmental State After Acute Kidney Injury

PROVIDER: PRJNA497279 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8071920_1.fastq.gz	Fastqsanger.gz
	SRR8071920_2.fastq.gz	Fastqsanger.gz
	SRR8071911_1.fastq.gz	Fastqsanger.gz
	SRR8071911_2.fastq.gz	Fastqsanger.gz
	SRR8071921_1.fastq.gz	Fastqsanger.gz

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Resident Macrophages Reprogram Toward a Developmental State After Acute Kidney Injury

Project description:Resident Macrophages Reprogram Toward a Developmental State After Acute Kidney Injury

| PRJNA497279 | ENA

Resident Macrophages Reprogram Toward a Developmental State After Acute Kidney Injury

Project description:Background – Acute kidney injury (AKI) is a devastating clinical condition affecting at least two-thirds of critically ill patients and among these patients is associated with a greater than 60% risk of mortality. Kidney mononuclear phagocytes (MP) are necessary for pathogenesis and healing in mouse models of AKI and thus have been the subject of investigation as potential targets for clinical interventions. Methods and Results – We have determined that, after injury, F4/80Hi-expressing kidney resident macrophages (KRM) are a distinct cellular subpopulation that does not differentiate from non-resident infiltrating MP. However, if KRM are depleted using polyinosinic:polycytidylic acid (poly I:C), they can be reconstituted from bone marrow derived precursors. Further, KRM lack major histocompatibility complex class II (MHCII) expression before post-parturition day 7 (P7) but upregulate it over the next 14 days. This MHCII- KRM phenotype reappears after injury. RNA sequencing shows injury causes transcriptional reprogramming of KRM to more closely resemble that found at P7. Post-injury KRM are also enriched in Wingless-type MMTV integration site family (Wnt) signaling, indicating a pathway vital for mouse and human kidney development is active. Conclusions – These data indicate that mechanisms involved in kidney development may be active after injury in KRM.

2019-04-16 | GSE121410 | GEO

Resident macrophages reprogram toward a developmental state after acute kidney injury.

Project description:Acute kidney injury (AKI) is a devastating clinical condition affecting at least two-thirds of critically ill patients, and, among these patients, it is associated with a greater than 60% risk of mortality. Kidney mononuclear phagocytes (MPs) are implicated in pathogenesis and healing in mouse models of AKI and, thus, have been the subject of investigation as potential targets for clinical intervention. We have determined that, after injury, F4/80hi-expressing kidney-resident macrophages (KRMs) are a distinct cellular subpopulation that does not differentiate from nonresident infiltrating MPs. However, if KRMs are depleted using polyinosinic/polycytidylic acid (poly I:C), they can be reconstituted from bone marrow-derived precursors. Further, KRMs lack major histocompatibility complex class II (MHCII) expression before P7 but upregulate it over the next 14 days. This MHCII- KRM phenotype reappears after injury. RNA sequencing shows that injury causes transcriptional reprogramming of KRMs such that they more closely resemble that found at P7. KRMs after injury are also enriched in Wingless-type MMTV integration site family (Wnt) signaling, indicating that a pathway vital for mouse and human kidney development is active. These data indicate that mechanisms involved in kidney development may be functioning after injury in KRMs.

| S-EPMC6413788 | biostudies-literature

Single cell RNA sequencing analysis of mouse resident and infiltrating immune cells during acute kidney injury and fibrosis

Project description:To obtain an unbiased characterization of the resident and infiltrating immune cell populations of mouse kidneys in healthy and diseased states, we performed single cell RNA-seq of facs-sorted CD45+ immune cells and CD4+ T cells from naïve and injured kidneys, at selected time points.

2020-01-31 | E-MTAB-8002 | biostudies-arrayexpress

Cx3cr1 controls kidney resident macrophage heterogeneity

Project description:Cx3cr1 controls kidney resident macrophage heterogeneity

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JAK2V617F-dependent clonal hematopoiesis drives vascular resident macrophages toward a pathogenic phenotype and promotes dissecting aortic aneurysm

Project description:JAK2V617F-dependent clonal hematopoiesis drives vascular resident macrophages toward a pathogenic phenotype and promotes dissecting aortic aneurysm

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p53? is a transcriptionally inactive p53 isoform able to reprogram cells toward a metastatic-like state.

Project description:Although much is known about the underlying mechanisms of p53 activity and regulation, the factors that influence the diversity and duration of p53 responses are not well understood. Here we describe a unique mode of p53 regulation involving alternative splicing of the TP53 gene. We found that the use of an alternative 3' splice site in intron 6 generates a unique p53 isoform, dubbed p53?. At the molecular level, p53? is unable to bind to DNA and does not transactivate canonical p53 target genes. However, like certain p53 gain-of-function mutants, p53? attenuates the expression of E-cadherin, induces expression of markers of the epithelial-mesenchymal transition, and enhances the motility and invasive capacity of cells through a unique mechanism involving the regulation of cyclophilin D activity, a component of the mitochondrial inner pore permeability. Hence, we propose that p53? encodes a separation-of-function isoform that, although lacking canonical p53 tumor suppressor/transcriptional activities, is able to induce a prometastatic program in a transcriptionally independent manner.

| S-EPMC4136628 | biostudies-literature

Human and Murine Kidneys Contain Transcriptionally and Spatially Orthologous Resident Macrophage Subpopulations in Acute Kidney Injury

Project description:Acute kidney injury (AKI) is a major health burden in the United States. Macrophages have been shown to mediate AKI in murine models. Murine kidneys contain multiple subpopulations of kidney resident macrophages (KRM) that are transcriptionally and spatially distinct. We hypothesized the human kidney contains orthologous KRM subpopulations, both transcriptionally and spatially. We utilized kidney sections from donors diagnosed with mild to moderate AKI in order to increase the translatability of murine research to clinical settings. We used spatial transcriptomics and single cell RNA sequencing to identify five distinct human KRM subpopulations. Using the AddModuleScore function in Seurat, we were able to compare the murine KRM transcriptional profiles from pre and post-AKI to the human KRM subpopulations. As a result, we identified four orthologous to known murine KRM subpopulations. The remaining population was identified in the kidney cortex and expresses a profile similar to activate microglia, the resident macrophage population in the brain. Again, we used AddModuleScore to determine a set of marker genes that will allow for the identification of KRM subsets across species and injury.

2024-03-01 | GSE226533 | GEO

Kidney-resident CD8 T cells downregulate IL-18R during maturation

Project description:Using the expression of IL-18 receptor (CD218) as a surface marker, CD69+ kidney-resident CD8 T cells can be separated into two subsets. Transcriptional analysis suggests that IL-18R low subset represents the mature tissue-resident T cells

2020-03-01 | GSE111801 | GEO

Cx3cr1 controls kidney resident macrophage heterogeneity

Project description:Kidney macrophages are comprised of both monocyte-derived and tissue resident populations; however, the heterogeneity of kidney macrophages and factors that regulate their heterogeneity are poorly understood. Herein, we performed single cell RNA sequencing (scRNAseq), fate mapping, and parabiosis to define the cellular heterogeneity of kidney macrophages in healthy mice. Our data indicate that healthy mouse kidneys contain four major subsets of monocytes and two major subsets of kidney resident macrophages (KRM) including a population with enriched Ccr2 expression, suggesting monocyte origin. Surprisingly, fate mapping data using the newly developed Ms4a3Cre Rosa Stopf/f TdT model indicate that less than 50% of Ccr2+ KRM are derived from Ly6chi monocytes. Instead, we find that Ccr2 expression in KRM reflects their spatial distribution as this cell population is almost exclusively found in the kidney cortex. We also identified Cx3cr1 as a gene that governs cortex specific accumulation of Ccr2+ KRM and show that loss of Ccr2+ KRM reduces the severity of cystic kidney disease in a mouse model where cysts are mainly localized to the kidney cortex. Collectively, our data indicate that Cx3cr1 regulates KRM heterogeneity and niche-specific disease progression.

2023-05-01 | GSE193892 | GEO

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