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Microarray-based clustering analysis of miRNAs altered in IRI-AKI mouse kidney

ABSTRACT: Microarray-based clustering analysis of miRNAs altered in IRI-AKI mouse kidney

PROVIDER: PRJNA721871 | ENA |

REPOSITORIES: ENA

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Microarray-based clustering analysis of miRNAs altered in IRI-AKI mouse kidney

Project description:The aim of this study was to identify miRNAs that regulate AKI and develop their applications as diagnostic biomarkers and therapeutic agents. First, kidney tissues from two different AKI mouse models, namely, AKI induced by the administration of lipopolysaccharide (LPS) causing sepsis (LPS-AKI mice) and AKI induced by renal ischemia–reperfusion injury (IRI-AKI mice), were exhaustively screened for their changes of miRNA expression compared with that of control mice by microarray analysis.

2021-05-14 | GSE172039 | GEO

Microarray-based clustering analysis of miRNAs altered in LPS-AKI mouse kidney

2021-05-14 | GSE172038 | GEO

Microarray-based clustering analysis of miRNAs altered in LPS-AKI mouse kidney

Project description:Microarray-based clustering analysis of miRNAs altered in LPS-AKI mouse kidney

| PRJNA721870 | ENA

Effects of GPX3-Specific Knockout in Renal Tubular Epithelial Cells on Kidney Gene Expression During the IRI-AKI Process

Project description:GPX3 is primarily synthesized and secreted by renal tubular epithelial cells and serves as the main source of GPX3 in plasma. A portion of GPX3 adheres to the renal basement membrane, suggesting that GPX3 may also regulate renal cell physiological functions. Our previous work has found that GPX3 expression is downregulated in the renal tubular epithelial cells of mice that have undergone ischemia-reperfusion-induced acute kidney injury, but the specific impact of this downregulation remains unclear. To address this, we constructed mice with specific deletion of GPX3 in renal tubular epithelial cells and subjected them to ischemia-reperfusion modeling. We reported the protective role of native GPX3 in the kidneys under IRI-AKI conditions in mitigating oxidative stress and mitochondrial damage in tubular epithelial cells. The deletion of GPX3 in tubular epithelial cells exacerbated oxidative stress, apoptosis, and mitochondrial dysfunction in IRI-AKI. Renal cortex tissue from control and IRI-modeled mice was used for RNA sequencing. Overall, our data provide an overview of the genetic changes in the kidneys of mice with GPX3 knockout in both non-modeled and IRI-AKI-modeled conditions, laying the groundwork for studying the specific mechanisms by which GPX3 regulates renal function.

2025-03-17 | GSE283852 | GEO

SUMO2/3 conjuagted proteins in kidney of IRI-AKI mice

Project description:the result of SUMO2/3 conjuagted proteins in kidney of IRI-AKI miceof using IP and LC-MS

2025-10-10 | PXD069295 |

The P2Y14/UDP-Glucose pathway is a therapeutic target for ischemic AKI

Project description:Ischemic acute kidney injury (AKI), a complication that frequently occurs in hospital settings, is often associated with hemodynamic compromise, sepsis, cardiac surgery or exposure to nephrotoxicants. AKI is associated with immune cell infiltration into the kidney stroma, which causes acute tubular injury. Here, using a murine renal ischemic-reperfusion injury (IRI) model we show that intercalated cells (ICs) rapidly adopt a pro-inflammatory phenotype post IRI. During the early phase of AKI, we demonstrate that either blocking the pro-inflammatory P2Y14 receptor located on the apical membrane of ICs, or ablation of the gene encoding the P2Y14 receptor in ICs: 1) inhibits IRI-induced chemokine expression increase in ICs; 2) reduces neutrophil and monocyte renal infiltration; 3) reduces the extent of kidney dysfunction; and 4) attenuates proximal tubule (PT) damage. These observations indicate that the P2Y14 receptor participates in the very first inflammatory steps associated with ischemic AKI. In addition, we show that the concentration of the P2Y14 receptor ligand, uridine diphosphate-glucose (UDP-Glc), is higher in urine samples from intensive care unit patients who developed AKI when compared with urine from patients without AKI. In particular, we observed a strong correlation between UDP-Glc concentration and the development of AKI in cardiac surgery patients. Our study identifies the UDP-Glc/P2Y14 receptor axis as a potential target for the prevention and/or attenuation of ischemic-AKI.

2020-03-17 | GSE144522 | GEO

Expression data from livers of female wild-type mice subjected to warm bilateral renal artery ischemia-reperfusion injury (RIR) in comparison to livers of female wild type mice subjected to sham surgery.

Project description:RIR leads to ischemic acute kidney injury (AKI). Women below the age of menopause have a lower incidence of AKI. It is bellieved that estrogens are protective. Many genes were shown to be altered in female wild-type mice subjected to IRI.

2019-10-17 | GSE138996 | GEO

Increased Elmo1 Expression worsens the AKI-CKD transition via ROS

Project description:Ischemia-reperfusion injury (IRI) is a major cause of acute kidney injury (AKI) and a key contributor to the progression toward chronic kidney disease (CKD), with oxidative stress playing a central role in this transition. Engulfment and Cell Motility 1 (ELMO1) regulates cytoskeletal remodeling and reactive oxygen species (ROS) production through RAC1 activation, yet its involvement in redox imbalance and kidney injury remains unclear. To investigate this, a unilateral renal IRI model was established in wild-type (WT) and ELMO1-overexpressing (Elmo1 H/H) mice. Renal function was evaluated using plasma cystatin C, estimated glomerular filtration rate (eGFR), and urinary albumin-to-creatinine ratio (UACR), while structural and ultrastructural kidney changes were assessed by Masson’s trichrome staining and electron microscopy. Redox-related gene expression was analyzed via RT-qPCR, and global transcriptional alterations were examined using RNA sequencing.

2025-12-09 | GSE304219 | GEO

Effects of GPX3-Specific Knockout in Renal Tubular Epithelial Cells on Kidney Gene Expression During the IRI-AKI Process

Project description:Effects of GPX3-Specific Knockout in Renal Tubular Epithelial Cells on Kidney Gene Expression During the IRI-AKI Process

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Extracellular Matrix Stiffness determines kidney metabolism reprogramming after AKI

Project description:Kidney repair after acute kidney injury (AKI) relies on a well-regulated extracellular matrix (ECM) that provides structural and mechanical cues. Fibroblasts and pericytes, key ECM producers, are rapidly activated post-injury, but ECM-driven repair mechanisms remain unclear. Using proteomics, spatial transcriptomics, and animal models, we profiled the landscape of matrix proteins altered post-AKI, highlighting microfibrillar-associated protein 2 (Mfap2) as a critical ECM component. Predominantly derived from fibroblasts and pericytes, Mfap2 loss impairs kidney architecture and metabolism, worsening AKI. Proteomics revealed that Mfap2 knockout suppresses tubule-derived Hmgcs2 via Esr2-mediated transcriptional repression and enhanced succinylation. Phosphoproteomics showed Mfap2 deletion hyperactivates MAPK and Lats1 in tubules, independent of integrin signaling and Yap/Taz. Mechanistically, reduced Lats1 boosts Esr2 transcription without affecting its degradation. Esr2 agonists restored kidney function in Mfap2-deficient models. Thus, Mfap2 governs ECM stiffness, transduces mechanical signals, reprograms metabolism, and fosters a pro-repair microenvironment critical for AKI recovery.

2025-12-23 | PXD064267 | Pride

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