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Transcriptome analysis of CMT64 cells following TGF-β and/or TNF-α treatment.

ABSTRACT: Transcriptome analysis of CMT64 cells following TGF-β and/or TNF-α treatment.

PROVIDER: PRJNA689310 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13344611_1.fastq.gz	Fastqsanger.gz
	SRR13344611_2.fastq.gz	Fastqsanger.gz
	SRR13344612_1.fastq.gz	Fastqsanger.gz
	SRR13344612_2.fastq.gz	Fastqsanger.gz
	SRR13344613_1.fastq.gz	Fastqsanger.gz

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Transcriptome analysis of CMT64 cells following TGF-β and/or TNF-α treatment.

Project description:We have previously demonstrated that TNF-α, a proinflammatory cytokine, enhances TGF-β-mediated EMT in A549 human lung cancer cells. RNA-sequencing analysis on CMT64 cells following TGF-β and/or TNF-α treatment revealed a subset of genes possibly regulated by TGF-β and/or TNF-α.

2021-12-13 | GSE164160 | GEO

Transcriptional effects of TNF-Î± and TGF-Î²1 on human umbilical vein endothelial cells

Project description:Transcriptional profiling of human umbilical vein endothelial cells following stimulation with tumour necrosis factor alpha and transforming growth factor beta singly or combined for 8 hr All stimulations were for 8 hr - TNF-Î± vs no cytokine; TGF-Î²1 vs no cytokine; TNF-Î± & TGF-Î²1 vs TNF-Î± alone; TNF-Î± & TGF-Î²1 vs TGF-Î²1 alone

2012-10-31 | E-GEOD-33416 | biostudies-arrayexpress

TGF or TNF Time series in ARPE19

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

Transcription profiling of Caco-2 and T84 human cell lines treated with flagellin, lymphotox beta or TNF alpha

Project description:14 day old Caco-2 and T84 cells were treated for 4 hours with flagellin, lymphotox beta or TNF alpha, respectively, and their expression profile compared to non-stimulated cells.

2007-08-04 | E-GEOD-1474 | biostudies-arrayexpress

Caco-2 and T84 cells stimulated with with flagellin, lymphotox beta or TNF alpha

Project description:14 day old Caco-2 and T84 cells were treated with flagellin, lymphotox beta or TNF alpha, respectively, and their expression profile compared to non-stimulated cells. Keywords: other

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NMuMG cell response to TGF-beta and TGF-beta +2APB treatments

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Transcriptional effects of TNF-α and TGF-β1 on human umbilical vein endothelial cells

2012-10-31 | GSE33416 | GEO

Effect of overexpression and depletion of MCEMP1 following stimulation of THP1 cells with TGF-beta

Project description:Effect of overexpression and depletion of MCEMP1 following stimulation of THP1 cells with TGF-beta

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Mice VSMCs: Control vs. TNF-α cultured

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The effects of terbutaline or GW9508 on TNF-alpha and IFN gamma (TNF-alpha + IFN gamma) stimulation by HaCaT

Project description:G-protein coupled receptors (GPCRs) have diverse roles in physiological processes, including immunity. Gs-coupled GPCRs increase while Gi-coupled ones decrease intracellular cAMP. Previous studies suggest that, in epithelial cells, Gs-coupled GPCRs enhance whereas Gi-coupled GPCRs suppress pro-inflammatory immune responses. In order to examine the issue, we chose beta2 adrenergic receptor and GPR40 as representatives of Gs- and Gi- coupled GPCRs, respectively, and examined their effects on TNF-alpha and IFN-gamma-(TNF-alpha + IFN-gamma) induced gene expression by HaCaT. We used microarrays to detail the global changes of gene expression induced by a beta2 adrenergic receptor agonist terbutaline or GPR40 agonist GW9508 pre-treatment in TNF-alpha + IFN-gamma - stimulated HaCaT cells. HaCaT cells were pre-treated with terbutaline or GW9508, TNF-alpha + IFN-gamma were then added, and cultured for another 24 h. Cells were then used for RNA extraction and hybridization on Affymetrix microarrays. We sought to clarify changes in gene expression after 1) TNF-alpha + IFN-gamma, 2) TNF-alpha + IFN-gamma + terbutaline, and 3) TNF-alpha + IFN-gamma + GW9508 treatment. To this end, we set 4 groups of samples; 1) unstimulated group, 2) TNF-alpha + IFN-gamma-stimulated group, 3) TNF-alpha + IFN-gamma + terbutaline-stimulated group, and 4) TNF-alpha + IFN-gamma + GW9508-stimulated group. In each group, HaCaT cells were stimulated in triplicate wells (n=3).

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