Expression data from RLT-PSC, human pancreatic stellate cell lineage
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE59953 | GEO | 2014/08/10
SECONDARY ACCESSION(S): PRJNA257164
REPOSITORIES: GEO
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Project description:Gene expression patterns in human PSCs exposed to chronic hyperglycemia with and without subsequent 48h TGF-β1 treatment or to TGF-B1 treatment alone. Treatments were compared to control human PSCs cultured in normal glucose concentration Total RNA was extracted from human PSCs of RLT-PSC line exposed to chronic hyperglycemia with or without subsequent TGF-β1 treatment and in PSCs exposed to 48h TGF-β1 treatment. Each treatment was compared to control human PSCs cultured in normal glucose concentration. Samples from all treatment arms were hybridized on Affymetrix PrimeView Human Gene Expression Array
2014-08-10 | E-GEOD-59953 | biostudies-arrayexpress
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2010-10-28 | GSE24965 | GEO
Project description:Tissue inhibitor of metalloproteinase 1 (TIMP-1) controls matrix metalloproteinase (MMP) activity through 1:1 stochiometric binding. Human TIMP-1 fused to a glycosylphosphatidylinositol (GPI) anchor (TIMP-1-GPI) shifts the activity of TIMP-1 from the extracellular matrix to the cell surface. TIMP-1-GPI treated renal cell carcinoma cells (RCC) show increased apoptosis and reduced proliferation. Transcriptomic profiling and regulatory pathway mapping were used to identify potential mechanisms driving these effects. Significant changes in inhibitor of DNA binding (IDs), TGF-β1/SMAD and BMP pathways resulted from TIMP-1-GPI treatment. These events were linked to reduced TGF-β1 signaling mediated by inhibition of proteolytic processing of latent TGF-β1 by TIMP-1-GPI. Activity of TIMP-1 from the extracellular matrix to the cell surface. TIMP-1-GPI treated renal cell carcinoma cells (RCC) show increased apoptosis and reduced proliferation. Transcriptomic profiling and regulatory pathway mapping were used to identify potential mechanisms driving these effects. Significant changes in inhibitor of DNA binding (IDs), TGF-β1/SMAD and BMP pathways resulted from TIMP-1-GPI treatment. These events were linked to reduced TGF-β1 signaling mediated by inhibition of proteolytic processing of latent TGF-β1 by TIMP-1-GPI. Renal cell carcinoma cells were transfected with empty vector, rhTimp1 and 2 concentrations of Timp1-GPI fusion protein
2012-08-23 | E-GEOD-40301 | biostudies-arrayexpress
Project description:Fibrotic diseases have significant health impact and have been associated with differentiation of the resident fibroblasts into myofibroblasts. In particular, stiffened extracellular matrix and TGF-β1 in fibrotic lesions have been shown to promote pathogenic myofibroblast activation and progression of fibrosis in various tissues. To better understand the roles of mechanical and chemical cues on myofibroblast differentiation and how they may crosstalk, we cultured primary valvular interstitial cells (VICs) isolated from porcine aortic valves and studied how traditional TCPS culture, which presents a non-physiologically stiff environment, and TGF-β1 affect native VIC phenotypes. We carried out gene expression profiling using porcine genome microarrays from Affymetrix and found that traditional TCPS culture induces major changes in gene expression of native VICs, rendering these cells more activated and similar to cells treated with TGF-β1. We also monitored time-dependent effects induced by TGF-β1 by examining gene expression changes induced by TGF-β1 at 8 hours and 24 hours. Porcine aortic VICs were isolated and cultured with or without TGF-β1 treatment for RNA extraction and hybridization on Affymetrix microarrays. We included 3 biological replicates for each condition. P0 VICs were freshly isolated cells which had not been cultured. P2 VICs were cells that had been passaged 2 times and cultured on plastic plates in low serum media. Some of the P2 VICs were treated with TGF-β1 at 5ng/ml for 8 hours or 24 hours. All the control and TGF-β1-treated conditions were collected at the same time on day 3 of culture.
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Project description:To elucidate the gene profile of anti-fibroproliferative effects of cyclosporine, we added TGF-b and/or CsA to MRC5 (fetal human lung fibroblast) cell line. After 24 hours serum starvation, fibroblasts were treated with 3 ng/ml TGF-β1 and were treated with or without 2μg/ml Cyclosporine and effects were examined at 48 hours after treatment. Expression of three genes (IGFBP3, ID1 and PPARG) from this signature was quantified in the same RNA samples by real-time PCR. TGF-β and cyclosporine induced gene expression data was measured in MRC5 (fetal human fibroblast cell line) at 48h after treatments. The dose of TGF-β was 3 ng/ml and cyclosporine was 2 μg/ml. The comparison was done between four groups (control, TGF-β, cyclosporine and TGF-β plus cyclosporine).Three independent experiments were performed at each treatments using different samples for each experiment.
2010-11-09 | E-GEOD-25200 | biostudies-arrayexpress
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Project description:Microarray analysis reveals up-regulation of retinoic acid and hepatocyte growth factor related signaling pathways by pro-insulin C-peptide in kidney proximal tubular cells: Antagonism of the pro-fibrotic effects of TGF-b1 Novel signaling roles for C-peptide have recently been discovered with evidence that it can ameliorate complications of type 1 diabetes. Here we sought to identify new pathways regulated by C-peptide of relevance to the pathophysiology of diabetic nephropathy. Microarray analysis was performed to identify genes regulated by either C-peptide and/or transforming growth factor beta 1 (TGF-β1) in a human proximal tubular cell line, HK-2. Expression of retinoic acid receptor β (RARβ), hepatcoyte growth factor (HGF), cellular retinoic acid binding protein II (CRABPII), vimentin, E-cadherin, Snail and β-catenin was assessed by immunoblotting. The cellular localisation of vimentin and β-catenin was determined by immunocytochemistry. Changes in cell morphology were assessed by phase contrast microscopy. Gene expression profiling demonstrated differential expression of 953 and 1,458 genes after C-peptide exposure for 18h or 48h respectively. From these, members of the anti-fibrotic retinoic acid (RA) and HGF signaling pathways were selected. Immunoblotting demonstrated that C-peptide increased RARβ, CRABPII and HGF. We confirmed a role for RA in reversal of TGF-β1-induced changes associated with epithelial-mesenchymal transition (EMT), including expression changes in Snail, E-cadherin, vimetin and redistribution of β-catenin. Importantly, these TGF-β1-induced changes were inhibited by C-peptide. Further, effects of TGF-β1 on Snail and E-cadherin expression were blocked by HGF and inhibitory effects of C-peptide were removed by blockade of HGF activity. This study identifies a novel role for HGF as an effector of C-peptide, possibly via an RA signaling pathway, highlighting C-peptide as a potential therapy for diabetic nephropathy.
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Project description:The etiology of autoimmune hepatitis is poorly understood but likely involves Th1 cells producing IFN-γ. BALB/c background TGF-β1-/- mice rapidly develop fulminant Th1-mediated autoimmune hepatitis. Our aims are to profile liver gene expression in TGF-β1-/- mice, to identify gene expression pathways dependent on IFN-γ as possible targets for rational therapy, and to test potential targets directly in vivo in mice. Keywords: Comparative analysis of gene expression in livers of WT, TGFB1 & IFN knockout mice DNA microarray analyses were applied to liver RNA from TGF-β1-/- mice, TGF-β1-/- /IFN-γ-/- mice, and TGF-β1+/+ littermate controls. 3 mice from each group were analyzed in this study.
2009-02-28 | E-GEOD-9892 | biostudies-arrayexpress
Project description:Members of the NADPH oxidase (NOX) family of enzymes, which catalyze the reduction of O2 to reactive oxygen species, have increased in number during eukaryotic evolution. Seven isoforms of the NOX gene family have been identified in mammals; however, specific roles of NOX enzymes in mammalian physiology and pathophysiology have not been fully elucidated. The best established physiological role of NOX enzymes is in host defense against pathogen invasion in diverse species, including plants. The prototypical member of this family, NOX-2 (gp91phox), is expressed in phagocytic cells and mediates microbicidal activities. Here we report a role for the NOX4 isoform in tissue repair functions of myofibroblasts and fibrogenesis. Transforming growth factor-β1 (TGF-β1) induces NOX-4 expression in lung mesenchymal cells by a SMAD-3–dependent mechanism. NOX-4–dependent generation of hydrogen peroxide (H2O2) is required for TGF-β1–induced myofibroblast differentiation, extracellular matrix (ECM) production and contractility. NOX-4 is upregulated in lungs of mice subjected to noninfectious injury and in cases of human idiopathic pulmonary fibrosis (IPF). Genetic or pharmacologic targeting of NOX-4 abrogates fibrogenesis in two murine models of lung injury. These studies support a function for NOX4 in tissue fibrogenesis and provide proof of concept for therapeutic targeting of NOX-4 in recalcitrant fibrotic disorders. Experiment Overall Design: mRNA expression of genes in human fetal lung mesenchymal cells (IMR-90) treated with or without TGF-β1, as analyzed by Affymetrix (U133A) microarrays. Control (C0, C2, C3) = cells without TGF-β1 treatment (n=3). Experimental (T0, T5, T7) = cells treated with TGF-β1 (2ng/ml) (n=3). mRNA was collected for all 6 samples for 48 hours post treatment.
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