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Alteration of renal gene expression following miR-22 inhibition in rhabdomyolysis (24 h) induced acute kidney injury

ABSTRACT: Alteration of renal gene expression following miR-22 inhibition in rhabdomyolysis (24 h) induced acute kidney injury

PROVIDER: PRJNA421167 | ENA |

REPOSITORIES: ENA

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Alteration of renal gene expression following miR-22 inhibition in rhabdomyolysis (24 h) induced acute kidney injury

Project description:In acute kidney injury (AKI) regions of the kidney are hypoxic. However, for reasons yet unknown, adaptation to hypoxia through hypoxia inducible factor (HIF) is limited. Here we seek for potential HIF repressors, their amenability to intervention, and assess the consequences for AKI outcome Renal miR-22 is up-regulated in AKI. In vitro, miR-22 is inducible by hypoxia, represses HIF, and this repression is offset by specific anti-miR-22 molecules. Inhibition of miR-22 in AKI leads to a complex regulation of more than 3,000 renal genes, most of which are unrelated to the HIF pathway.

2019-11-20 | GSE107710 | GEO

Comparison of the transcriptomic profiles of WT and complement C3-deficient mice with rhabdomyolysis-induced acute kidney injury

Project description:Rhabdomyolysis is a severe condition caused by skeletal muscle damage, leading to acute kidney injury (AKI). We demonstrate that complement has a direct pathogenic role in rhabdomyolysis-induced AKI. Deposition of C3d in the tubules of patients and mice correlated with rhabdomyolysis-induced AKI. Moreover, C3-defiient mice with rhabdomyolysis had preserved renal function. Mechanistically, C3-deficiency attenuated strongly inflammatory and apoptotic components of the renal transcriptome, perturbed by rhabdomyolysis. Complement was activated intrarenal by the lectin pathway via collectin-11. It proceeded in a C4-bypass manner and was amplified by heme-activated alternative pathway. Therefore, complement and heme are promising therapeutic targets for rhabdomyolysis-induced AKI.

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Transcriptome analysis of muscle in horses suffering from recurrent exertional rhabdomyolysis revealed energetic pathway alterations and disruption in the cytoplasmic calcium regulation

Project description:The purpose of this study was to compare the gene expression profile of recurent exercise rhabdomyolysis vs control muscles in French Trotter to determine any metabolic or structural disorder. Transcriptome analysis revealed 191 genes significantly modulated in rhabdomyolysis vs control muscles (p<0.05). Many genes involved in the fatty acid oxidation, the TCA cycle and the mitochondrial respiratory chain were severely down-regulated. The muscle fibers were under hypoxia and oxidative stress conditions which stimulated glycolysis. The muscle fiber calcium homeostasis was greatly affected towards an increase of cytoplasmic calcium and a depletion of the sarcoplasmic reticulum calcium. Gene expression analysis revealed an alteration of the aerobic ATP synthesis with a severe mitochondrial dysfunction which could explain the disruption of the cytoplasmic calcium regulation and a muscular relaxation disorder. Total RNA was extracted from the gluteal medius and longissimus lumborum muscles after biopsies in 15 French Trotter horses including 10 controls and 5 RER horses affected by rhabdomyolysis with high plasmatic muscular enzyme activities. Gene expression analysis was performed on the muscle biopsies using a 25K oligonucleotide microarray.

2010-12-15 | E-GEOD-26047 | biostudies-arrayexpress

Multi-omics characterization of recurrent exertional rhabdomyolysis in Standardbred horses

Project description:During an episode of acute rhabdomyolysis, a microarray study identified differential expression of calcium-regulatory, mitochondrial and metabolic genes in gluteal muscle of Standardbreds. Whether this represents expression related to acute myodegeneration or a specific molecular signature of susceptibility to recurrent exertional rhabdomyolysis (RER) is currently unknown. We compared gluteal muscle histopathology, gene/protein expression and antioxidant concentrations between Standardbreds with a history of, but not currently experiencing rhabdomyolysis, and race-trained controls to derive a molecular susceptibility profile.

2023-03-11 | PXD026121 | Pride

Transcriptome analysis of muscle in horses suffering from recurrent exertional rhabdomyolysis revealed energetic pathway alterations and disruption in the cytoplasmic calcium regulation

2010-12-15 | GSE26047 | GEO

Gene expression of single cell of rhabdomyolysis induced acute kidney injury cells

Project description:We used single cell RNA sequencing to identify the immune cells and especially mononuclear phagocytic cells affecting rhabdomyolysis induced acute kidney injury.

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Transcriptomic analysis of rhabdomyolysis induced kidney injury

Project description:Acute kidney injury (AKI) represents a syndrome seldom characterized by a single, distinct pathophysiological cause. Rhabdomyolysis-induced acute kidney injury (RIAKI) constitutes roughly 15% of AKI cases, yet its underlying pathophysiology remains poorly understood. Using a murine model of RIAKI induced by muscular glycerol injection, we aimed to analyse transcriptomic alterations by RNAseq.

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SOX9 promotes stress-responsive transcription of VGF nerve growth factor inducible gene in renal tubular epithelial cells

Project description:Acute kidney injury (AKI) is a common clinical condition associated with diverse etiologies and abrupt loss of renal function. In patients with sepsis, rhabdomyolysis, cancer, as well as cardiovascular disorders, the underlying disease or associated therapeutic interventions can cause hypoxic, cytotoxic, and inflammatory insults to renal tubular epithelial cells (RTECs) resulting in the onset of AKI. To uncover stress-responsive disease-modifying genes, here we have carried out renal transcriptome profiling in three distinct murine models of AKI. We find that Vgf nerve growth factor inducible gene upregulation is a common transcriptional stress response in RTECs to ischemia, cisplatin, and rhabdomyolysis-associated renal injury. The Vgf gene encodes a secretory peptide precursor protein that has critical neuro-endocrine functions; however, its role in the kidneys remains unknown. Our functional studies show that RTEC-specific Vgf gene ablation exacerbates ischemia, cisplatin, and rhabdomyolysis-associated AKI in vivo and cisplatin-induced RTEC cell death in vitro. Importantly, addback experiments showed that aggravation of cisplatin-induced renal injury caused by Vgf gene ablation is partly reversed by TLQP-21, a Vgf-derived peptide. Finally, in vitro and in vivo mechanistic studies showed that injury-induced Vgf upregulation in RTECs is driven by the transcriptional regulator Sox9. These findings identify Vgf as an essential stress-responsive gene and reveal a crucial molecular target of the Sox9 regulated transcriptional program that controls epithelial cell fate during AKI.

2020-09-03 | GSE153625 | GEO

A large germline alteration affecting MAX and FUT8, causing familial bilateral malignant pheochromocytoma and renal oncocytoma

Project description:Familial pheochromocytoma (PCC) has been associated with germline mutations in 14 genes. Here we investigated three siblings, who presented with (metastatic) bilateral pheochromocytomas, renal oncocytoma, and erythrocytosis. By SNP-array on one patient’s germline DNA a large complex genomic alteration was identified encompassing the intragenic and promoter regions of Myc-Associated Factor X (MAX) and alpha-(1,6)-fucosyltransferase (FUT8). The alteration was confirmed in all patients, as well as loss of the wild type MAX and FUT8 alleles and corresponding loss of protein expression. Uniparental disomy of chromosome 14q, previously demonstrated as a hallmark for MAX-related PCC, was also shown in the index patient by SNP-array. Our results indicate that large genomic deletions of MAX should be considered in familial and bilateral PCC with prior negative testing for gene mutations. In addition, MAX appears to be a new tumor suppressor gene for renal oncocytomas. SNP array was performed for 2 samples: 1 tumor DNA sample and 1 corresponding germline DNA sample

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Transcriptomic analysis of rhabdomyolysis induced kidney injury

Project description:Transcriptomic analysis of rhabdomyolysis induced kidney injury

| PRJNA1103748 | ENA