Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA95947 | ENA |
REPOSITORIES: ENA
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Project description:Idiopathic pulmonary fibrosis (IPF) is a refractory and lethal interstitial lung disease; EBV has previously been localised to alveolar epithelial cells of IPF patients. The molecular process of the epithelial mesenchymal transition (EMT) in IPF remains still unknown. Using an oligonucleotide array analysis, we observed dysregulated expression of members of non-canonical Wnt family in EBV infected A549 after TGF?1 exposure. TGF?1 exposure induced EMT increasing ?-Smooth Muscle Actin (ACTC) and Wnt5b gene expression, but decreasing E-cadherin and DKK1. When data were analyzed as a function of Wnt5b in EMT, significance differences in ACTC and E-cadherin gene expression, active TGF?1 protein levels and collagen deposition could be detected. Treatment with 9-cis Retinoic Acid (9-cisRA) significantly inhibited Wnt5b expression in both EBV infected and non-infected A549, followed by decreased collagen deposition and active TGF?1 protein level. Specific non-canonical Wnt-signalling genes are dysregulated in EBV infected cells and A549 treated with TGF?1; while, 9-cisRA treatment appears to attenuate EMT process in vitro. Experiment Overall Design: EBV infected cells and A549 were cultured in RPMI1640+5%FCS, and exposed to 10ng/ml TGF beta1 for 4hours. RNA isolation, cDNA synthesis, in vitro transcription and microarray analysis were performed as previously reported (Kieran et al., 2003). All analysis were microarrayed in duplicate. Image files were obtained through Affymetrix GeneChip software (MAS5), subsequently robust multichip analysis (RMA) was performed. Expression data were compared to control, p<0.05 correlated values and a signal log ratio of 0.6 or greater (equivalent to a fold change in expression of 1.5 or greater) were taken to identify significant differential regulation (Bolstad et al., 2003). All the SLRs data resulting from the comparative analyses in duplicate were reported in a scatter plot graph to determine the reliability of the assay and the linearity by r2. For all the microarray assays r2 value was higher than 0.98. Using normalised RMA values by Gene Cluster Software, Average Linkage Hierarchical Cluster Analysis was performed using TreeView analysis software (Eisen et al., 1998). Lists of dysregulated genes in both TGF?1 exposed cell lines were curated via the publicly available DAVID, Gene-Ontology (GOCharts) and Functional Annotation Clustering databases (Dennis et al., 2003).
2008-06-13 | E-GEOD-5457 | biostudies-arrayexpress
Project description:TGF-beta1 effect on human osteosarcoma cell line MNNG/HOS
| PRJNA167380 | ENA
Project description:Alveolar type II (ATII) epithelial cells function as stem cells, contributing to alveolar renewal, repair and cancer. Therefore, they are a highly relevant model for studying lung diseases, including acute injury, fibrosis and cancer, in which signals transduced by RAS and transforming growth factor (TGF)-ß play critical roles. To identify downstream molecular events following RAS and/or TGF-ß activation, we performed proteomic analysis using a quantitative label-free approach (LC-HDMSE) to provide in-depth proteome coverage and estimates of protein concentration in absolute amounts. Contact: pjss@soton.ac.uk
2021-02-04 | PXD023720 | Pride
Project description:Idiopathic pulmonary fibrosis (IPF) is a refractory and lethal interstitial lung disease; EBV has previously been localised to alveolar epithelial cells of IPF patients. The molecular process of the epithelial mesenchymal transition (EMT) in IPF remains still unknown. Using an oligonucleotide array analysis, we observed dysregulated expression of members of non-canonical Wnt family in EBV infected A549 after TGF?1 exposure. TGF?1 exposure induced EMT increasing ?-Smooth Muscle Actin (ACTC) and Wnt5b gene expression, but decreasing E-cadherin and DKK1. When data were analyzed as a function of Wnt5b in EMT, significance differences in ACTC and E-cadherin gene expression, active TGF?1 protein levels and collagen deposition could be detected. Treatment with 9-cis Retinoic Acid (9-cisRA) significantly inhibited Wnt5b expression in both EBV infected and non-infected A549, followed by decreased collagen deposition and active TGF?1 protein level. Specific non-canonical Wnt-signalling genes are dysregulated in EBV infected cells and A549 treated with TGF?1; while, 9-cisRA treatment appears to attenuate EMT process in vitro. Keywords: EBV infection, EMT and non-canonical Wnt pathway in A549 detected by oligonucleotide array
2006-08-05 | GSE5457 | GEO
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
Project description:TGF-beta1 target genes in human dendritic cells (DC).
| PRJNA104283 | ENA
Project description:TGF-beta1-Induced Gene Expression Changes in HepG2 Cells
| PRJNA196711 | ENA
Project description:Multipotent progenitors (MPP) and common dendritic cell progenitors (CDP) were obtained from mouse bone marrow, followed by in vitro culture with a specific cytokine cocktail and FACS sorting (Felker et al., 2010; Sere et al., 2012). Cells were treated with 10 ng/ml recombinant human TGF-b1 (R&D Systems, Minneapolis, USA) for 2, 4, 8, 12 and 24 h as described (Felker et al., 2010) or left untreated. Untreated multipotent progenitor (MPP) - MPP_0h_1 - MPP_0h_2 - MPP_0h_3 TGF-beta1 treated (2 hours) MPP - MPP_2h_1 - MPP_2h_2 - MPP_2h_3 TGF-beta1 treated (4 hours) MPP - MPP_4h_1 - MPP_4h_2 - MPP_4h_3 TGF-beta1 treated (8 hours) MPP - MPP_8h_1 - MPP_8h_2 - MPP_8h_3 TGF-beta1 treated (12 hours) MPP - MPP_12h_1 - MPP_12h_2 - MPP_12h_3 TGF-beta1 treated (24 hours) MPP - MPP_24h_1 - MPP_24h_2 - MPP_24h_3 Untreated common dendritic cell progenitor (CDP) - CDP_0h_1 - CDP_0h_2 - CDP_0h_3 TGF-beta1 treated (2 hours) CDP - CDP_2h_1 - CDP_2h_2 - CDP_2h_3 TGF-beta1 treated (4 hours) CDP - CDP_4h_1 - CDP_4h_2 - CDP_4h_3 TGF-beta1 treated (8 hours) CDP - CDP_8h_1 - CDP_8h_2 - CDP_8h_3 TGF-beta1 treated (12 hours) CDP - CDP_12h_1 - CDP_12h_2 - CDP_12h_3 TGF-beta1 treated (24 hours) CDP - CDP_24h_1 - CDP_24h_2 - CDP_24h_3
2014-04-15 | E-GEOD-46109 | biostudies-arrayexpress
Project description:Pulmonary fibrosis (PF) is associated with many chronic lung diseases including Systemic sclerosis (SSc), Idiopathic Pulmonary Fibrosis (IPF) and Cystic Fibrosis (CF) which are characterized by the progressive accumulation of stromal cells and formation of scar tissue. Pulmonary fibrosis is a dysregulated response to alveolar injury which causes a progressive decline in lung function and refractory to current pharmacological therapies. Airway and alveolar epithelial cells and stromal cells contribute to pulmonary fibrosis but the cell-specific pathways and gene networks that are responsible for the pathophysiology are unknown. Recent animals models generated in our lab demonstrate clinical phenotypes seen in human fibrotic disease. The mouse model of transforming growth factor-? (TGF?)-induced fibrosis include conditionally expressing TGF? in the lung epithelium under control of the CCSP promoter driving rtTA expression (CCSP/TGF?). This allow the TGF? is only expressed in airway and alveolar epithelial cells and only when mice fed doxycycline (Dox). Similar to PF in humans, TGF? mice on Dox developed a progressive and extensive adventitial, interstitial and pleural fibrosis with a decline in lung mechanics. Thus, the TGF? transgenic mouse is a powerful model to determine lung cell-specific molecular signatures involved in pulmonary fibrosis. In this study, we sought to determine changes in the transcriptome during TGF?-induced pulmonary fibrosis. Our results showed that several pro-fibrotic genes increased in the lungs of TGF? mice. This study demonstrates that WT1 network gene changes associated with fibrosis and myfibroblast accumulation and thus may serve as a critical regulator fibrotic lung disease. mRNA profiles of CCSP/- and CCSP/TGFalpha mice treated with Dox
2015-03-07 | E-GEOD-66634 | biostudies-arrayexpress