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ST2+ T-regulatory Cells in Renal Inflammation and Fibrosis following Ischemic Kidney Injury

ABSTRACT: The role of IL-33 and its receptor ST2 in kidney injury is not well understood. This study demonstrates the importance of ST2 expression on the T-regulatory cells (Tregs) for the resolution of renal injury by suppressing inflammation and fibrosis. Treg-specific deletion of ST2, detrimentally impacted late outcomes of renal injury worsening the impairment of kidney function, inflammation, and fibrosis.

ORGANISM(S): Mus musculus

PROVIDER: GSE272380 | GEO | 2024/08/27

REPOSITORIES: GEO

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ST2+ T-regulatory Cells in Renal Inflammation and Fibrosis following Ischemic Kidney Injury

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ST2+ T-regulatory Cells in Renal Inflammation and Fibrosis following Ischemic Kidney Injury

Project description:Here, we delineated the role of the ST2 specifically in Treg cells, using murine renal injury models and kidney organoids.

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Single-cell sequencing reveals Mincle receptor mediated inflammation for resolution in ischemic kidney injury

Project description:Recent studies have demonstrated a strong association between acute kidney injury (AKI) and chronic kidney disease (CKD), while the unresolved inflammation is believed to be a driving force for this chronic transition process. As a transmembrane pattern recognition receptor, Mincle (macrophage-inducible C-type lectin, Clec4e) was identified to participate in the early immune response after AKI. However, the impact of Mincle on the chronic transition of AKI remains largely unclear. We performed single-cell RNA sequencing (scRNA-seq) with the unilateral ischemia-reperfusion (UIR) murine model of AKI at days 1, 3, 14 and 28 after injury. Potential effects and mechanism of Mincle on renal inflammation and fibrosis were further validated in vivo utilizing Mincle knockout mice. The dynamic expression of Mincle in macrophages and neutrophils throughout the transition from AKI to CKD was observed. For both cell types, Mincle expression was significantly up-regulated on day 1 following AKI, with a second rise observed on day 14. Notably, we identified distinct subclusters of Mincle-high neutrophils and Mincle-high macrophages that exhibited time-dependent influx with dual peaks characterized with remarkable pro-inflammatory and pro-fibrotic functions. Moreover, we identified that Mincle-high neutrophils represented an "aged" mature neutrophil subset derived from the "young" mature neutrophil cluster in kidney. Additionally, we observed a synergistic mechanism whereby Mincle-expressing macrophages and neutrophils sustained renal inflammation by augmenting tumor necrosis factor (TNF) production. Mincle-deficient mice exhibited reduced renal injury and fibrosis following AKI.

2024-05-23 | GSE267242 | GEO

Cortical kidney bulk RNA Sequencing in the reversible unilateral ureter obstruction model.

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Role of ST2 expession in regulatory Tcells on muscle regneration

Project description:We describe the effects of Treg ST2 expression on muscle regeneration. We compare regneration from cryo-injured tibialis anterior muscle from Foxp3-Cre/ST2-flox vs Foxp3-Cre mice 8 days post-injury. These analyses from whole muscle provide insight into the role of muscle Tregs in the context of regeneration. The tibialis anterior muscle from male Foxp3-Cre/ST2 flox or Foxp3-Cre/ST2 WT C57BL/6 mice (2 months old) were cryo-injured using a liquid nitrogen chilled metal probe for 8 seconds. 8 days post-injury whole muscle was harvested and snap frozen in liquid nitrogen. Whole muscle was then homogenized directly in TriZol and gene expression profiling was performed on Affymetrix Mouse Gene 1.0 ST Arrays.

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Quantitative proteomic analysis of the role of knocking down NRP1 after OGD/R in primary renal tubular epithelial cells

Project description:Neuropilin-1 (NRP1), a co-receptor for various cytokines, including TGF-β, has been identified as a potential therapeutic target for fibrosis. However, its role and mechanism in renal fibrosis remains elusive. Here, we show that NRP1 is upregulated in distal tubular (DT) cells of patients with transplant renal insufficiency and mice with renal ischemia-reperfusion (I-R) injury. Knockout of Nrp1 reduced multiple endpoints of renal injury and fibrosis. We found that Nrp1 facilitates the binding of TNF-α to its receptor in DT cells after renal injury. This signaling results in a downregulation of lysine crotonylation of the metabolic enzyme Cox4i1, decreased cellular energetics and exacerbation of renal injury. Furthermore, by single-cell RNA-sequencing we found that Nrp1-positive DT cells secrete collagen and communicate with myofibroblasts, exacerbating acute kidney injury (AKI)-induced renal fibrosis by activating Smad3. Dual genetic deletion of Nrp1 and Tgfbr1 in DT cells better improves renal injury and fibrosis than either single knockout. Together, these results reveal that targeting of NRP1 represents a promising strategy for the treatment of AKI and subsequent chronic kidney disease

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Proteomic experiment of lysine crotonylation modification to analysis of the role of knocking down NRP1 after IR in kidney

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RNAseq of kidneys from a mice model of chronic leptospirosis infection and induced a secondary nephrotoxic injury by adenine feeding

Project description:Background The mysterious chronic kidney disease is multifactorial causes. One of the risk factors is leptospirosis, a re-emerging infectious disease caused by Leptospira spp., for endemic leptospirosis tend to coincide with high-incidence regions of chronic kidney disease of unknown etiology. This study aims to investigate the role of leptospirosis as an emerging culprit in which chronic subclinical kidney injury, may predispose to progressive kidney disease when superimposed on secondary nephrotoxic injury. Methods Adenine-induced renal injury in chronic leptospira-infected C57/BL6 mice were studied for evaluating the renal function, histology and gene expression changes. We employed RNA sequencing-based renal transcriptome to investigate pathogenic pathways associated with secondary nephrotoxic injury in chronic kidney injury due to leptospirosis. Results The severity of kidney lesions was increased and the expression of immune/inflammation/fibrosis genes were significantly up-regulated in either low-dose (0.1%) and high-dose (0.2%) adenine-induced renal injury superimposed on infected mice. Whole renal transcriptome analysis reveals that the substantial amplification of the tremendous amount of expressed genes and fibrosis-related pathways was found in adenine-induced kidney injury add-on to leptospira-infected mice which correlated with kidney dysfunction and fibrosis compared to infection or adenine itself. A total of 41 differentially expressed genes associated with fibrosis were identified in infected mice fed with adenine, suggesting that these potential genes contributed to aggravated renal progression occurred in adenine-fed chronic leptospira-infected mice. Conclusions In summary, this study indicates that chronic subclinical kidney infection when exposed to different degree of secondary nephrotoxic injury may predispose to exacerbated and progressive chronic kidney disease.

2021-04-05 | GSE150641 | GEO

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2014-06-09 | E-GEOD-54417 | biostudies-arrayexpress

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