Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1327852 | ENA |
REPOSITORIES: ENA
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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: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 Role of SOX9 in hypoxia/reoxygenation (H/R) injuried mice primary renal tubular epithelial cells Purpose: we performed comparative RNA-seq analyses to identify differentially expressed genes between Knockdown of Sox9 and negtive control in hypoxia/reoxygenation (H/R) injuried mice primary renal tubular epithelial cells. Methods:we grew mouse primary renal tubular epithelial cells to approximately 50% confluence, transfected using EndoFectin™ Max (GeneCopoeia, China) 12h before suffering to H/R injury. H/R was used to mimic IRI in vitro. Briefly, cells were incubated in glucose-free medium in a tri-gas incubator (94% N2, 5% CO2 and 1.0% O2) at 37 °C for 6 hours. Subsequently, cells were incubated in complete medium under normal conditions for 18 hours for reoxygenation. Cells were then collected by 1ml TRIzol (Invitrogen, Carlsbad), and sent to Annoroad Corporation (Beijing, China) for high throughout Illumina NovaSeq 6000 sequencing (GPL24247) (Illumina, San Diego, CA, USA). Results: To determine the possible pathways of Sox9 in protecting mice primary renal tubular epithelial cells from injury, we conduct the transcriptomotic sequencing. After sequence, the clean reads rate of all samples were ≥98%.The quality of the assembled transcriptome is good enough for functional annotation and further analysis. Conclusions: We performed RNA-sequencing (RNA-Seq) on isolated mouse renal tubular epithelial cells of two groups, treated with H/R and transfected with siNC (H/R+siNC group) or siSox9 (H/R+siSox9 group). SOX9-responsive genes showed significant enrichment of the WNT signaling pathway in primary tubular epithelial cells.
2022-12-19 | GSE174811 | GEO
Project description:The Role of EGR1 in hypoxia/reoxygenation (H/R) injuried mice primary renal tubular epithelial cells Purpose: we performed comparative RNA-seq analyses to identify differentially expressed genes between Knockdown of Egr1 and negtive control in hypoxia/reoxygenation (H/R) injuried mice primary renal tubular epithelial cells. Methods:we grew mouse primary renal tubular epithelial cells to approximately 50% confluence, transfected using EndoFectin™ Max (GeneCopoeia, China). H/R was used to mimic IRI in vitro. Briefly, cells were incubated in glucose-free medium in a tri-gas incubator (94% N2, 5% CO2 and 1.0% O2) at 37 °C for 6 hours. Subsequently, cells were incubated in complete medium under normal conditions for 18 hours for reoxygenation. Cells were then collected by 1ml TRIzol (Invitrogen, Carlsbad), and sent to Annoroad Corporation (Beijing, China) for high throughout Illumina NovaSeq 6000 sequencing (GPL24247) (Illumina, San Diego, CA, USA). Results: To determine the possible pathways and downregulated genes of Egr1 in protecting mice primary renal tubular epithelial cells from injury, we conduct the transcriptomotic sequencing. After sequence, the clean reads rate of all samples were ≥98%.The quality of the assembled transcriptome is good enough for functional annotation and further analysis. Conclusions: We performed RNA-sequencing (RNA-Seq) on isolated mouse renal tubular epithelial cells of 3 groups, negtive control(Sham group) treated with H/R (H/R group) or Egr1 overexpression plasmid (Egr1OV group). Egr1-responsive genes showed significant enrichment in proliferation pathway.
2022-12-19 | GSE174808 | GEO
Project description:Mutations in PKD1 cause Autosomal Dominant Polycystic Kidney Disease (ADPKD). To further investigate the impact of Pkd1 knockout on renal tubular cells, a direct reprogramming approach was applied. After direct reprogramming of mouse embryonic fibroblasts to induced renal tubular epithelial cells (iRECs), Pkd1 knockout iREC clones were generated by Cre-mediated recombination of floxed Pkd1 alleles. The knockout clones were compared to their corresponding wild type clones by RNA Sequencing and transcriptome profiling.
2022-11-22 | GSE148840 | GEO
Project description:To understand the transcription regulation of renal tubular epithelial cells under stimuli, here we investigated transcriptome, chromatin accessibility and their dynamics through RNA-seq and ATAC-seq under the three types of treatments. We identified genome-wide functional regions which coordinated transcription regulation in human renal proximal tubule epithelial cells (HK2). Our results provide a cell type-specific landscape of chromatin dynamics under stimuli and discovered an important TF in renal tubular epithelial cells that mediated genomic response to different injury stimuli.
2022-01-01 | GSE150042 | GEO
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
Project description:Renal epithelial cells are exposed to mechanical forces due to flow-induced shear stress within the nephrons. We applied RNA sequencing to get a comprehensive overview of fluid-shear regulated genes and pathways in the immortalized renal proximal tubular epithelial cell line. Cells were exposed to laminar fluid shear stress (1.9 dyn/cm2) in a cone-plate device and compared to static controls.
2018-03-15 | E-MTAB-6640 | biostudies-arrayexpress