Similar Datasets
Project description:HK2 gene expression in response to osmolytes
| PRJNA668117 | ENA
Project description:Aristolochic acid nephropathy (AAN) is characterised by rapidly progressive tubulointerstitial nephritis culminating in end stage renal failure and urothelial malignancy. microRNAs (miRs) are small endogenous post-transcriptional regulators of gene expression implicated in numerous physiological and pathological processes. We aimed to characterise the mechanism of AA induced cell cycle arrest and its regulation by miRs. The microarray experiment was performed to identify differentially regulated microRNAs in human proximal tubulal epithelial cells treated with aristolochic acid (AA). Analysis or differential miR expression in human proximal tubular epithelial cell line (HK-2) treated with 5ug/ml aristolochic acid, control (n=3) vs aristolochic acid (n=3)
2014-01-09 | E-GEOD-53911 | biostudies-arrayexpress
Project description:In order to identify the effects of OCRL depletion on the proximal tubular renal cells transcriptome, we performed Affymetrix Gene-Chip hybridization experiments Transcriptome analysis of the proximal tubular cells depleted of OCRL
2016-12-20 | GSE54284 | GEO
Project description:Induced renal epithelial cells were obtained by direct reprogramming of murine fibroblasts. Their expression profile was compared to control fibroblasts and primary renal tubular epithelial cells.
2016-07-01 | E-MTAB-3648 | biostudies-arrayexpress
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: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.
2014-06-09 | GSE54417 | 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
Project description:The impact of canagliflozin on gene expression changes was investigated in human renal proximal tubular cells (HK2) after pre-treatment with high glucose.
2019-02-27 | GSE106156 | GEO
Project description:Pkd1-/- 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 Pkd1-/- 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.
2019-03-01 | E-MTAB-6641 | biostudies-arrayexpress
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