E-GEOD-15205
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ABSTRACT:
PROVIDER: E-GEOD-15205 | ExpressionAtlas | 2015-09-02
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:The purpose of this study is to determine the changes in gene expression by a human retinal pigment epithelium (RPE) cell line (ARPE-19) in response to combination treatment of TGF and TNF, which induces phenotypic changes in vitro that mimic the EMT (Epithelial-to-Mesenchymal Transition). For this purpose, total RNA was extracted from TGF and TNF-treated ARPE-19 cells and differential gene expression between each time point (0, 1, 6, 16, 24, 42, and 60 hours) was determined using genechip arrays (Affymetrix, Human Genome U133). Experiment Overall Design: ARPE19 cell lines treated with TGF and TNF for 0, 1, 6, 16, 24, 42, and 60 hour. Each experiment were repeated three times. But 1 hour experiment was repeated two times.
2009-09-15 | E-GEOD-12548 | biostudies-arrayexpress
Project description:The purpose of this study is to determine the changes in gene expression by a human retinal pigment epithelium (RPE) cell line (ARPE-19) in response to combination treatment of TGF and TNF, which induces phenotypic changes in vitro that mimic the EMT (Epithelial-to-Mesenchymal Transition). For this purpose, total RNA was extracted from TGF and TNF-treated ARPE-19 cells and differential gene expression between each time point (0, 1, 6, 16, 24, 42, and 60 hours) was determined using genechip arrays (Affymetrix, Human Genome U133). Keywords: time course
2009-08-26 | GSE12548 | GEO
Project description:Aberrant epithelial-mesenchymal transition (EMT) is involved in pathological processes including fibrotic disorders and cancer invasion and metastasis. Alterations of the cell-extracellular matrix (ECM) interaction also contribute to those pathological settings. However, the functional interplay between EMT and cell-ECM interaction is poorly understood. Here, we show that tumor necrosis factor (TNF)-alpha, a potent mediator of inflammation, induces EMT-associated fibrosis in retinal pigment epithelial cells, and that this is regulated by hyaluronan (HA)-CD44-Moesin interaction. TNF-alpha elicits both HA synthesis and Moesin phosphorylation through protein kinase C activation, promoting binding of CD44 to the newly synthesized HA. The HA-CD44-Moesin interaction leads to cell-cell dissociation through actin remodeling and increased cellular motility associated with mesenchymal phenotype. Furthermore, we established an in vivo model of TNF-alpha-induced fibrosis in the mouse eye, and the ocular fibrosis was completely suppressed in CD44-null mice. Therefore, HA production and its interaction with CD44 plays essential role in TNF-alpha-induced-EMT, and the interference of the complex formation can be a new strategy for the fibrotic disorders. ARPE19 cell lines were treated with TGF and TNF for 6 and 42 hour. Each experiment were repeated three times. But 1hour experiment was repeated two times. For this submission, total RNA was extracted from TGF- or TNF-treated ARPE-19 cells and differential gene expression between each time point (6 and 42 hours) was determined using genechip arrays (Affymetrix, Human Genome U133).
2010-03-23 | E-GEOD-15205 | biostudies-arrayexpress
Project description:Transcriptome analysis of RNAs extracted from 2 hour-TGF-b-treated or untreated LX-2 cells with or without STAT3 knockdown We prepared RNA from the following groups: NS 0h: untreated cells with control non-silencing (NS) siRNA; NS 2h: 2-hour TGF-b treated cells with control NS siRNA; siSTAT3 0h: untreated cells with STAT3 siRNA; siSTAT3 2h: 2-hour TGF-b treated cells with STAT3 siRNA. The gene expression profiles were compared, and we found 202 genes were upregulated (fold > 1.5) upon TGF-b treatment in control NS siRNA transfected LX-2 cells. Among them, 128 genes were clasified as TGF-b-induced and STAT3 -dependent genes as their response to TGF-b decreased more than 40% upon STAT3 depletion (126 genes) or fold between NS control and siSTAT3 in the absence of TGF-b was > 1.5 (2 genes). The results showed that STAT3 plays an important role in regulating TGF-b target genes.
2017-02-07 | GSE92638 | GEO
Project description:Gene expression profile of A549 cells treated with TGF-beta
| PRJNA563653 | ENA
Project description:Gene expression signitures in ARPE-19 cells treated with or without TGF-β1
| PRJNA414473 | ENA
Project description:To identify the dysregulated lncRNA and mRNA expression in ARPE-19 cells underwent EMT, we established a TGF-β1 induced EMT model of ARPE-19 cells. ARPE-19 cells were treated with or without 10 ng/ml TGF-β1 for 48 h. Total RNA are extracted and subjected to microarray assay (Arraystar Human LncRNA Microarray V3.0)
2021-08-11 | GSE105053 | GEO
Project description:Gene expression profile of human peritoneal mesothelial cells (HPMC) treated with TGF-b1
| PRJNA497194 | ENA
Project description:1,7-bis(4-hydroxy-3-methoxyphenyl)heptane-3,5-dione (tetrahydrocurcumin, THC) is a major bioactive metabolite of curcumin (the principal active ingredient of Curcuma longa L.), and overcomes the low bioavailability of curcumin, demonstrating the potential anti-inflammatory, antioxidant and neuroprotective properties, etc, some of which were considered to be even superior to curcumin. In the present study, the protective properties of THC in the hippocampus of APP/PS1 mice, and the effects of THC against Aβ-induced toxicity in BV-2 cells were explored. The data in vitro showed that Aβ induced decreased cell viability, and cell cycle arrest and apoptosis in BV-2 cells, which could be ameliorated by THC. In vivo, THC administration was able to rescue learning and memory, and reduce Aβ burden in the hippocampus of APP/PS1 mice. By comprehensive proteomic analysis of the hippocampus of mice, a total of 157 differentially expressed proteins were identified in APP/PS1 mice treated with THC (comparing with APP/PS1 mice), which were enriched in “T cell activation”, “lymphocyte proliferation” and “protein oligomerization”, etc. The results of Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis suggested that the effects of THC on the cell cycle and apoptosis were mostly related to the “Ras signaling pathway” and “JAK−STAT signaling pathway”, etc. Using Western blot and ELISA, the down-regulation of Gab2 and K-Ras, and the up-regulation of caspase-3, TGF-β1 and TNF-ɑ were found in APP/PS1 mice. THC attenuated the abnormal expression of Gab2, K-Ras, caspase-3 and TNF-ɑ, and up-regulated Bag1 and TGF-β1 expression in APP/PS1 mice. In BV-2 cells, Aβ induced the down-regulation of Gab2, K-Ras and TGF-β1, and the overexpression of caspase-3, PARP1, cleaved-PARP1 and TNF-ɑ, which were markedly restored by THC. Moreover, THC up-regulated Bag1 expression in BV-2 cells treated with Aβ. The decreased transcriptional expression levels of Ccnd2 and Cdkn1a was also observed in Aβ-treated BV-2 cells. THC treatment alleviated down-regulation of Ccnd2, but did not affect the abnormal transcriptional expression of Cdkn1a caused by Aβ in BV-2 cells. For the first time, we identified that the action of THC in preventing AD was associated with inhibition of cell cycle arrest and apoptosis of microglia via the Ras/ERK signaling pathway, shedding new light on the role of THC in alleviating the progression of AD.
2021-07-13 | PXD024721 | Pride
Project description:Purpose: to study the correlations between transcriptional signatures reflecting the abundance and functional activity of tumor-infiltrating inflammatory cells from RNA-seq data on one hand, and the number of intratumoral activated regulatory T lymphocytes Methods: Gene expression profiles of 19 snap-frozen cutaneous metastases from 19 melanoma patients were obtained by RNA-seq of poly-A RNA. Cryosections from the same tumors were stained by multiplexed immunofluorescence for GARP and FoxP3. FoxP3+GARP+ activated regulatory T lymphocytes (Treg) were quantified by computerized image analysis. Correlations between the proportion of activated Treg and gene expression signatures of inflammatory cells and pathways were analyzed by Gene Set Enrichment Analysis. Results: The genes whose expression level correlated the most with the proportion of activated Tregs were significantly enriched for genes expressed by T lymphocytes and for genes induced by IFN-gamma, TNF-alpha, IL-1-beta and TGF-beta, including genes induced by TGF-beta in effector T cells. Conclusions: Our results in this small series of melanoma samples suggest that Treg infiltration and Treg-dependent TGF-beta activity are proportional to T-cell infiltration and effector activity in tumors.
2020-06-27 | GSE153388 | GEO