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Arginase-1 is Required for Macrophage-Mediated Renal Tubule Regeneration

ABSTRACT: Arginase-1 is Required for Macrophage-Mediated Renal Tubule Regeneration

PROVIDER: PRJNA780907 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16958498.fastq.gz	Fastqsanger.gz
	SRR16958499.fastq.gz	Fastqsanger.gz

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Arginase-1 Is Required for Macrophage-Mediated Renal Tubule Regeneration.

Project description:BackgroundAfter kidney injury, macrophages transition from initial proinflammatory activation to a proreparative phenotype characterized by expression of arginase-1 (Arg1), mannose receptor 1 (Mrc1), and macrophage scavenger receptor 1 (Msr1). The mechanism by which these alternatively activated macrophages promote repair is unknown.MethodsWe characterized the macrophage and renal responses after ischemia-reperfusion injury with contralateral nephrectomy in LysM-Cre;Arg1fl/fl mice and littermate controls and used in vitro coculture of macrophages and tubular cells to determine how macrophage-expressed arginase-1 promotes kidney repair.ResultsAfter ischemia-reperfusion injury with contralateral nephrectomy, Arg1-expressing macrophages were almost exclusively located in the outer stripe of the medulla adjacent to injured S3 tubule segments containing luminal debris or casts. Macrophage Arg1 expression was reduced by more than 90% in injured LysM-Cre;Arg1fl/fl mice, resulting in decreased mouse survival, decreased renal tubular cell proliferation and decreased renal repair compared with littermate controls. In vitro studies demonstrate that tubular cells exposed apically to dead cell debris secrete high levels of GM-CSF and induce reparative macrophage activation, with those macrophages in turn secreting Arg1-dependent factor(s) that directly stimulate tubular cell proliferation.ConclusionsGM-CSF-induced, proreparative macrophages express arginase-1, which is required for the S3 tubular cell proliferative response that promotes renal repair after ischemia-reperfusion injury.

| S-EPMC9161787 | biostudies-literature

Arginase-1 is Required for Macrophage-Mediated Renal Tubule Regeneration

Project description:In this study, we compared the transcriptomes of the kidney subjected to unilateral IRI with contralateral nephrectomy (IRI/CL-NX) and the normal healthy control kidney at the single cell level to identify major cell types in the kidney and the differential transcriptional response during kidney repair following IRI.

2022-03-23 | GSE188966 | GEO

RNA-seq profiling of microdissected rat renal tubule segments

Project description:We sequenced mRNAs from glomeruli and 14 different rat renal tubule segments collected by hand microdissection. Collagenase-digested rat renal tubule segments were collected by hand microdissection. Poly(A)-mRNAs were captured from cell lysate and sequenced using paired-end protocol.

2015-03-31 | E-GEOD-56743 | biostudies-arrayexpress

Inhibition of prolyl hydroxylase promotes the reprogramming of Sox9+ renal progenitor cells and renal regeneration

Project description:Mammalian kidney has very limited ability to repair or regenerate after acute kidney injury (AKI). The maladaptive repair of AKI promotes the progression to chronic kidney disease (CKD). Therefore, it is extremely urgent to explore new strategies to promote the repair/regeneration of injured renal tubules after AKI. It has been shown that hypoxia induces heart regeneration in adult mice. However, it is unknown whether hypoxia can induce kidney regeneration after AKI. In this study, we used a prolyl hydroxylase domain inhibitor (PHDI), MK-8617, to mimic hypoxia condition and found that MK-8617 significantly ameliorates ischemia reperfusion injury (IRI) induced acute kidney injury. We then showed that MK-8617 dramatically facilitates renal regeneration via promoting the proliferation of injured renal proximal tubular cells (RPTCs) after IRI-induced AKI. We then performed bulk mRNA sequencing and discovered that multiple nephrogenesis- related genes were significantly upregulated with MK-8617 pretreatment. Furthermore, we showed that MK-8617 may alleviate proximal tubule injury via stabilizing HIF-1α protein specifically in renal proximal tubular cells. We also demonstrated that MK-8617 promotes the reprogramming of renal proximal tubular cells to Sox9+ renal progenitor cells, and the regeneration of renal proximal tubules. In summary, we discovered that inhibition of prolyl hydroxylase improves renal proximal tubule regeneration after IRI-induced AKI via promoting the reprogramming of renal proximal tubular cells to Sox9+ renal progenitor cells.

2024-10-10 | GSE247560 | GEO

Histone tail modification profiles of human renal tubule epithelial cells

Project description:To annotate the regulatory elements in the renal tubule epithelial cells, we profiled 6 histone ChIP-seq in the human kidney epithelical cells (HKC8). We pulled down the DNA with specific antibodies of interests against histone tail modifications in the human rebal tubule epithelial cells. The result can be interpretated with ChromHMM for different states.

2013-08-09 | E-GEOD-49637 | biostudies-arrayexpress

Transcription profiling of adult drosophila renal tubule vs whole fly

Project description:The experiment was designed to identify genes abundant or enriched in adult Drosophila melanogaster Malpighian (renal) tubule as compared to the whole fly.

2004-06-23 | E-MEXP-127 | biostudies-arrayexpress

WT1+ parietal epithelial progenitor cells are essential for renal proximal tubule repair and regeneration

Project description:WT1+ parietal epithelial progenitor cells are essential for renal proximal tubule repair and regeneration

| PRJNA765339 | ENA

RNA-seq profiling of microdissected rat renal tubule segments

Project description:We sequenced mRNAs from glomeruli and 14 different rat renal tubule segments collected by hand microdissection.

2015-03-31 | GSE56743 | GEO

Dysfunction of the circadian clock in the renal tubule leads to enhanced renal gluconeogenesis and exacerbated hyperglycemia in diabetes

Project description:In diabetes, the kidney contributes to the development of diabetic hyperglycemia by increasing glucose reabsorption from the primary urine and by upregulating gluconeogenesis in the proximal tubule. However, these two processes are also controlled by the circadian clock, a mechanism that synchronizes a large number of specific renal functions with environmental daily cycles. Here, we investigated the (patho)physiological role of intrinsic renal tubule circadian clocks in the diabetic kidney. We demonstrate that diabetic mice devoid of the circadian transcriptional regulator BMAL1 in the renal tubule exhibit additional enhancement of renal gluconeogenesis, exacerbated hyperglycemia, increased glucosuria, polyuria and renal hypertrophy. Collectively, our results suggest that diabetic hyperglycemia can be worsened by dysfunction or misalignment of intrinsic renal circadian clocks.

2022-05-27 | GSE178319 | GEO

WT1+ parietal epithelial progenitor cells are essential for renal proximal tubule repair and regeneration

Project description:Purpose: We have found that WT1+ parietal epithelial progenitor cells contribute to renal proximal tubule repair and regeneration by cell lineage tracing and direct differentiation analysis, but the transcription profile of these WT1+ PECs is largely unkown. Here, we aimed to unveil the transcriptional features of WT1+ PECs through single-cell RNA sequencing (scRNA-seq). Methods: Single cell suspension was prepared from kidney cortex of WT1CreERT2; Rosa26-tdTfl/+ mice that underwent sham or ischemic reperfusion injury (IRI) 24h .TdT+ cells were enriched by fluorescence activated cell sorter (FACS) and further analyzed with BD Rhapsody platform. Results: After quality control and cell filtering, 26,759 cells were informative (Dataset S1) and divided into 10 clusters using Harmony algorithm to reduce batch effects. GO analysis and QuSAGE heatmap suggested that WT1+ PECs might promote kidney regeneration after AKI through TGF-β and Notch signaling pathway. Marker gene expression analysis showed that WT1+ PECs shared the characteristics of STCs. Pseudotemporal analysis indicated that that WT1+ PECs developed to PTECs through STCs intermediate stage. Conclusions: scRNA-seq indicated that the rare, quiescent PECs supplied PTECs through STCs intermediate stage after severe ischemic injury, and this process most likely was regulated through TGF-β and Notch signaling pathway.

2023-03-22 | GSE184601 | GEO

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