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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

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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.

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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.

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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.

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Expression data from adult rat subventricular zone cells

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Expression data from adult rat subventricular zone cells

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Expression data from adult rat subventricular zone cells

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Alveolar Epithelial Cell Injury with EBV Upregulates TGF-beta1 Expression

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