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TGFß1-driven epithelial to mesenchymal transition in human kidney cell line

ABSTRACT: TGFbeta is the major cytokine driver of fibrosis in the kidney and other tissue. Epithelial-mesenchymal transition has been postulated to contibrute to renal fibrosis in diseases such as diabetic nephropathy. We wished to identify novel genes that were upregulated in human kidney epithelial cells in response to TGFb1.The transcriptional responses for human proximal tubule epithelial cells to 10 ng/ml TGFbeta1 was examined over 24 and 48 hr

ORGANISM(S): Homo sapiens

PROVIDER: GSE23338 | GEO | 2011/05/31

SECONDARY ACCESSION(S): PRJNA131473

REPOSITORIES: GEO

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TGFß1-driven epithelial to mesenchymal transition in human kidney cell line

Project description:TGFbeta is the major cytokine driver of fibrosis in the kidney and other tissue. Epithelial-mesenchymal transition has been postulated to contibrute to renal fibrosis in diseases such as diabetic nephropathy. We wished to identify novel genes that were upregulated in human kidney epithelial cells in response to TGFb1.The transcriptional responses for human proximal tubule epithelial cells to 10 ng/ml TGFbeta1 was examined over 24 and 48 hr There were three treatment groups: vehicle, 24hr TGFb1, 48 hr TGFb1. Each treatment was carried out in triplicate 10 cm plates and the experiment was carried out in triplicate using consecutive passages of cells.

2011-05-30 | E-GEOD-23338 | biostudies-arrayexpress

Jagged1/Notch2 controls kidney fibrosis via Tfam-mediated metabolic reprogramming

Project description:While Notch signaling has been proposed to play a key role in fibrosis, the direct molecular pathways targeted by Notch signaling and the precise ligand and receptor pair that are responsible for kidney disease remain poorly defined. In this study, we found that JAG1 and NOTCH2 showed the strongest correlation with the degree of interstitial fibrosis in a genome wide expression analysis of a large cohort of human kidney samples. Transcript analysis of mouse kidney disease models, including folic-acid-induced nephropathy, unilateral ureteral obstruction, or APOL1-associated kidney disease, indicated that Jag1 and Notch2 levels were higher in all analyzed kidney fibrosis models. Mice with tubule-specific deletion of Jag1 or Notch2 (Kspcre/Jag1flox/flox and Kspcre/Notch2flox/flox) had no kidney-specific alterations at baseline, but showed protection from folic acid induced kidney fibrosis. Tubule-specific genetic deletion of Notch1 and global knock-out of Notch3 had no effect on fibrosis. In vitro chromatin immunoprecipitation experiments and genome-wide expression studies identified the mitochondrial transcription factor A (Tfam) as a direct Notch target. Re-expression of Tfam in tubule cells prevented Notch-induced metabolic and profibrotic reprogramming. Kidney tubule specific deletion of Tfam resulted in fibrosis. In summary, Jag1/Notch2 plays a key role in kidney fibrosis development by regulating Tfam expression and metabolic reprogramming.

2018-12-31 | GSE118600 | GEO

Transcription profiling of primary human tubular epithelial cells (HUTEC) response to TGFbeta at three concentrations to study the epithelial to mesenchymal transition

Project description:This experiment was aimed to study the Epithelial to mesenchimal transition (EMT) induced by TGFbeta in primary tubular epithelial cells. Primary cultures were grown for 4 days using three different TGFbeta1 concentrations: 5 ng/ml, 10 ng/ml and 50 ng/ml. Cells were grown in plastic flasks (Falcon) or in plastic flasks (Falcon) covered by type I collagen. Differentially expressed genes were identified comparing treated vs. control cells maintained for 4 days in 1% serum without TGFbeta1.

2006-12-31 | E-MEXP-566 | biostudies-arrayexpress

Expression data from adult rat subventricular zone cells

Project description:Transforming growth factor (TGF)-ß1 is a multifunctional cytokine regulating a number of physiological and patho-physiological processes in the adult brain. Its expression is elevated during neurodegeneration, which is associated with reduced levels of neurogenesis. We have postulated that TGF-ß1 might be one of the crucial factors involved in limiting neurogenesis in the diseased brain. We used microarrays to detail the gene expression profile after TGFbeta-1 treatment and identified distinct classes of up- and downregulated genes. Keywords: control versus TGFbeta1 treated group Adult rat subventricular zone cells were cultured for 7 days under proliferation conditions. Control cells were exposed to HCl/BSA whereas TGFbeta-1 treated cells received 10 ng/ml TGFbeta-1 dissolved in HCl/BSA 3 times per week. RNA was extracted followed by hybridization on Affymetrix microarrays.

2011-05-10 | E-GEOD-14556 | biostudies-arrayexpress

Expression data from adult rat subventricular zone cells

2011-05-10 | E-GEOD-14562 | biostudies-arrayexpress

Expression data from adult rat subventricular zone cells

2011-05-10 | GSE14562 | GEO

Expression data from adult rat subventricular zone cells

2011-05-10 | GSE14556 | GEO

Translational profiling of proximal tubule in fibrotic kidney

Project description:Injury to the proximal tubule plays a central role in the initiation and progression of kidney fibrosis, and rates of chronic kidney disease progresses approximately 50% faster in males compared to females. We applied Translating Ribosome Affinity Purification (TRAP) followed by RNA-sequencing to characterize the cell-specific proximal tubule transcriptional landscape during fibrosis in male vs. female mice.

2019-09-21 | GSE125015 | GEO

Alveolar Epithelial Cell Injury with EBV Upregulates TGF-beta1 Expression

Project description:Idiopathic pulmonary fibrosis (IPF) is a refractory and lethal interstitial lung disease characterized by alveolar epithelial cells apoptosis, fibroblast proliferation and extra-cellular matrix proteins deposition. Epstein - Barr virus (EBV) has previously been localised to alveolar epithelial cells of IPF patients. In this study we utilised a microarray based differential gene expression analysis strategy to identify potential molecular drivers of EBV associated lung fibrosis. We employed an alveolar epithelial cell line infected with EBV (A-Akata). Lytic phase infection induced in the A-Akata cells by TPA/BA treatment resulted in increase of TGFbeta1 and TIEG1 mRNA expression. Treatment of the A-Akata cells with ganciclovir, resulted in a down regulation of both TIEG1 and TGFbeta1 expression, accompanied by a suppression of the EBV early response genes, Rta and Zta. This suppression of cell turnover mediators was correlated with an increase in cell activity index. To identify a possible role for Rta in driving apoptotic gene expression, we inhibited the Rta gene expression by silencing RNA, resulting in a decrease in TGFbeta1 and TIEG1 expression. This study identifies an apoptotic role of the EBV early response genes, as enhancer factors of TIEG1 and TGFbeta1 in EBV infected alveolar epithelial cells, potentially providing a possible mechanism for the role of EBV infection in pulmonary fibrosis. Keywords: EBV lytic phase infection, epithelial cell apoptosis, oligonucleotide array analysis

2006-08-04 | GSE5450 | GEO

Single-Nucleus RNA Sequencing Identifies New Classes of Proximal Tubular Epithelial Cells in Kidney Fibrosis

Project description:The study used a clinically relevant mouse model of chronic aristolochic acid nephropathy (AAN) to investigate the responses of proximal tubular cells during kidney fibrosis by single-nucleus RNA sequencing. The experiment involved 4 mice with AAN induced chronic renal fibrosis and 4 naive controls.

2021-06-23 | E-MTAB-9390 | biostudies-arrayexpress

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