Microarray-based clustering analysis of miRNAs altered in IRI-AKI mouse kidney
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PROVIDER: PRJNA721871 | ENA |
REPOSITORIES: ENA
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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.
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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.
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Project description:Microarray-based clustering analysis of miRNAs altered in LPS-AKI mouse kidney
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Project description:Ischemia Reperfusion Injury-related Acute Kidney Injury (IRI-AKI) is a significant clinical challenge characterized by interrupted blood flow to the kidneys, leading to substantial complications such as prolonged hospital stays, chronic kidney disease, and increased mortality rates. Current management strategies are limited to supportive care, underscoring the need for targeted therapies. This study investigates the potential of Mesenchymal Stromal Cells (MSCs) to transfer functional mitochondria to damaged renal cells via gap junctions, specifically connexin 43 (Cx43), in a clinically relevant surgical model of IRI-AKI. We conducted a time-course analysis to identify critical time points for mitochondrial dysfunction and the optimal therapeutic window for MSC administration, comparing the reno-protective effects of bone marrow-derived MSCs (BM-MSCs) and umbilical cord-derived MSCs (UC-MSCs) in both in vivo and in vitro models. Additionally, we explored the activation of mitochondrial biogenesis and dynamics signaling pathways, particularly PGC1α, to assess the restoration of mitochondrial homeostasis in IRI-AKI, and its potential to disrupt the oxidative stress-inflammation axis, paving the way for precision therapies in treating IRI-AKI.
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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.
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Project description:Acute kidney injury (AKI), a condition marked by rapid loss of kidney function, carries significant morbidity and often progresses to chronic kidney disease (CKD). Ischemia-reperfusion injury (IRI) is a major pathogenic driver of AKI. To elucidate the molecular mechanisms underlying IRI-induced AKI and its progression to CKD, we performed comprehensive proteomic and phosphoproteomic profiling of kidney tissues. Using high-resolution mass spectrometry, we confidently quantified over 7,500 proteins and 4,400 non-redundant phosphoproteins, providing a systems-level view of the extensively remodeled kidney proteome and phosphoproteome post-IRI. Our dataset reveals dynamic alterations in key signaling pathways associated with AKI-to-CKD transition, offering unprecedented molecular insights into disease progression. This resource will facilitate the discovery of therapeutic targets to mitigate IRI-induced kidney damage and its chronic sequelae.
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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.
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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.
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