Ontology highlight
ABSTRACT:
PROVIDER: PRJNA609362 | ENA |
REPOSITORIES: ENA
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Project description:Aged-related kidney impairment that involves tubular epithelial cell senescence and renal fibrosis become a severe threaten for worldwide public health. m6A-mRNA epitranscriptomic microarray was performed to reveal the targeted genes with abnormal m6A modification in aged human kidney tissues.
2024-12-09 | GSE232249 | GEO
Project description:In order to study the effect of mesenchymal stem cells on miRNAs in renal tubular epithelial cells during renal fibrosis, and to find new treatment methods for renal fibrosis, we used TGF-β1 to stimulate mouse tubular epithelial cells, co-cultured with mesenchymal stem cells for 48 hours, and collected renal tubular epithelial cells .The renal tubular epithelial cells that were only stimulated by TGF-β1 were used as a control group. High-throughput miRNA sequencing was used to detect the increased and decreased miRNAs after co-culture.
2020-04-07 | GSE148144 | GEO
Project description:Sepsis is a severe and dysregulated inflammatory disease that often precedes the development of acute kidney injury (AKI) with consequent worsening outcome. The main characteristics of sepsis-induced AKI include endothelial cell (EC) dysfunction, infiltration of inflammatory cells, glomerular thrombosis, and renal tubular epithelial cells (RTEC) injury. Numerous studies have demonstrated that mammalian target of rapamycin (mTOR) activation has been implicated in the initiation and progression of renal injury in course of sepsis. However, little is known, about the molecular basis of mTOR role in EC and RTEC dysfunction. Here, we evaluate whether mTOR inhibition by Rapamycin (Rp) as potential strategy to ameliorate renal function and dissected the molecular mechanisms involved. In a mouse model of lipopolysaccharide (LPS)-induced AKI , LPS injection led to a time-dependent increase of serum creatinine and significant morphological changes in renal parenchyma associated with increased collagen deposits and endothelial dysfunction. Interestingly, Rp treatment significantly decreased creatine levels and preserved renal parenchyma, counteracting Endothelial-to mesenchymal transition (EndMT) process and early fibrosis through the inhibition of ERK pathway. Next, we examined the effects of LPS-TLR4 interaction in RTECs. Through a whole-genome DNA methylation analysis in cultured RTEC, we found that LPS induced aberrant methylation, particularly in regions involved in premature aging. The most represented genes were CD39 and WFS1. LPS stimulation of RTEC led to up-regulation of SA-β Gal and cell cycle arrest markers such as p21. In accordance, in endotoxemic mice, we found a decreased expression of CD39 concurrent with Klotho down-regulation. Administration of Rp exerted anti-aging effects in endotoxemic mice, preserving CD39 and Klotho expression. In conclusion, we demonstrated that mTOR inhibition could offer novel strategies to protect endothelial and tubular compartment from accelerated aging and fibrosis thus counteracting the progression to chronic kidney disease.
2024-09-16 | E-MTAB-13396 | biostudies-arrayexpress
Project description:The circadian clock has been found to be associated with various diseases. We showed that 5/6 nephrectomy (5/6Nx) Clk/Clk mice, which show mutation in the gene encoding circadian locomotor output cycles (Clock) do not show aggravation of renal fibrosis because transforming growth factor-1 (Tgf-1) expression is not increased. In wild-type 5/6Nx kidneys, we found that retinoid, a metabolite of retinol, led to alteration of the expresion 24-h rhythm of Clock expression. Renal Tgf- 1 expression is activated by Clock and further aggravates renal dysfunction by causing fibrosis. We also showed that, in 5/6Nx mice fed a retinol-free diet, renal fibrosis and apoptosis are reduced, leading to a marked improvement in serum creatinine levels. Moreover, our study identified hepatic Cyp3a11 and Cyp26a1 as key retinol metabolism-related genes whose expression decreased in 5/6Nx mice. Our data indicated that the negative chain reaction of metabolic clock alteration in between the kidney and liver aggravates renal dysfunction.
2014-06-06 | GSE57799 | GEO
Project description:Shiga toxin type 2 (Stx2) from Escherichia coli is thought to be a main factor to casue renal dysfunction in Enterohemorrhagic E. coli (EHEC) infection. The renal dysfunction caused by the proximal tubular defects can be detected in the earlier EHEC infection. However, the precise information of gene expression from proximal tubular epithelial cells has yet to be clarified. We performed microarray experiments using Stx2-injected mouse kidney and Stx2-treated human renal proximal tubular epithelial cells (RPTEC), and extracted common genes that were differentially expressed.
2022-01-01 | GSE172466 | GEO
Project description:Shiga toxin type 2 (Stx2) from Escherichia coli is thought to be a main factor to casue renal dysfunction in Enterohemorrhagic E. coli (EHEC) infection. The renal dysfunction caused by the proximal tubular defects can be detected in the earlier EHEC infection. However, the precise information of gene expression from proximal tubular epithelial cells has yet to be clarified. We performed microarray experiments using Stx2-injected mouse kidney and Stx2-treated human renal proximal tubular epithelial cells (RPTEC), and extracted common genes that were differentially expressed.
2022-01-01 | GSE172465 | GEO
Project description:A Gene Expression Signature that Predicts the Future Onset of Drug-Induced Renal Tubular Toxicity These data support the publication titled "A Gene Expression Signature that Predicts the Future Onset of Drug-Induced Renal Tubular Toxicity" Copyright (c) 2005 by Iconix Pharmaceuticals, Inc. Guidelines for commercial use: http://www.iconixbiosciences.com/guidelineCommUse.pdf replicated drug treatments with controls
2005-11-30 | E-GEOD-3210 | biostudies-arrayexpress
Project description:After LAPTM5 was overexpressed in rat renal tubular epithelial cells (NRK52E), proteomic sequencing was performed to analyze aging and fibrosis protein changes.
2024-06-05 | PXD052845 |
Project description:The mechanistic target of rapamycin mTORC1 is a key regulator of cell metabolism and autophagy. Despite widespread clinical use of mTOR inhibitors, the role of mTORC1 in renal tubular function and kidney homeostasis remains elusive. By utilizing constitutive and inducible deletion of conditional Raptor alleles in renal tubular epithelial cells, we discovered that mTORC1 deficiency caused a marked concentrating defect, loss of tubular cells and slowly progressive renal fibrosis. Transcriptional profiling revealed that mTORC1 maintains renal tubular homeostasis by controlling mitochondrial metabolism and biogenesis as well as transcellular transport processes involved in counter-current multiplication and urine concentration. Although mTORC2 partially compensated the loss of mTORC1, exposure to ischemia and reperfusion injury exaggerated the tubular damage in mTORC1-deficient mice, and caused pronounced apoptosis, diminished proliferation rates and delayed recovery. These findings identify mTORC1 as an essential regulator of tubular energy metabolism and as a crucial component of ischemic stress responses. Pharmacological inhibition of mTORC1 likely affects tubular homeostasis, and may be particularly deleterious if the kidney is exposed to acute injury. Furthermore, the combined inhibition of mTORC1 and mTORC2 may increase the susceptibility to renal damage. Raptor fl/fl*KspCre and Raptor fl/fl animals were sacrificed at P14 before the development of an overt functional phenotype. Kidneys were split in half and immediately snap frozen in liquid nitrogen.
2014-06-09 | E-GEOD-54417 | biostudies-arrayexpress
Project description:Renal fibrosis is an important pathological change in the development of progressive kidney diseases. Ubiquitination is a post-translational modification of proteins involved in the regulation of various pathophysiological processes. In this study, we found that the deubiquitinating enzyme YOD1 is significantly upregulated in the kidney tissues of Ang II-challenged mice and Ang II upregulates YOD1 expression in renal tubular epithelial cells. YOD1 deficiency significantly alleviated renal injury and fibrosis induced by Ang II infusion in mice. Mechanistically, RNA-seq and co-immunoprecipitation analysis showed a pro-fibrotic protein, JAK2, as a YOD1-binding protein. We identify that JAK2 interacts with the C-terminal Znf domain of YOD1. YOD1 removed K48-linked ubiquitination of JAK2 at residue K970 via its active site C155, which stabilizes JAK2 and then maintains JAK2/STAT3 signaling pathway activation to induce pro-fibrotic gene expression in renal tubular epithelial cells. JAK2 inhibitors reversed the renal fibrosis promoted by YOD1 in mice. We also show increased levels of YOD1 and JAK2 in the kidney tissues of patients with renal fibrosis. In addition, YOD1 knockout significantly prevents unilateral ureteral ligation (UUO)-induced renal fibrosis in mice. Collectively, these findings identify YOD1 as a novel regulator in renal fibrosis via deubiquitinating JAK2.
2024-01-06 | GSE234355 | GEO