Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effects of 4 mixture of cytokines including TNF-alpha, IL-1beta IFN-gamma, and TGF-bata1 on rhematoid arthritis synovial fibroblasts

ABSTRACT: To investigate effects of 4 mixture of cytokines including TNF-alpha, IL-1beta IFN-gamma, and TGF-bata1 on rhematoid arthritis synovial fibroblasts (RASFs), we treated RASFs (n = 3) with TNF-alpha (1 ng/mL), IL-1beta (0.1 ng/mL), IFN-gamma (10 ng /mL), TGF-beta1 (1 ng/mL) (4mix) or vehicle control (Veh) for 24 hours and conducted RNA-seq analysis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE305533 | GEO | 2026/08/15

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other
	GSE305533_Average_counts_All_samples.xlsx.xlsx	Xlsx

Items per page:

1 - 2 of 2

Similar Datasets

Effects of TEAD4 knockdown on rhematoid arthritis synovial fibroblasts stimulated with 4 mixture of cytokines including TNF-alpha, IL-1beta IFN-gamma, and TGF-bata1

Project description:To investigate effects of TEAD4 knockdown on rhematoid arthritis synovial fibroblasts (RASFs) stimulated with 4 mixture of cytokines including TNF-alpha, IL-1beta IFN-gamma, and TGF-bata1 , we pre-treated RASFs (n = 3) with siControl (siCtrl) or siTEAD4 for 72 hours, and then treated them with TNF-alpha (1 ng/mL), IL-1beta (0.1 ng/mL), IFN-gamma (10 ng /mL), TGF-beta1 (1 ng/mL) (4mix) for 24 hours and conducted RNA-seq analysis.

2026-08-15 | GSE305532 | GEO

Effects of GLI1, GLI3, and GLI1/3 knockdown on rhematoid arthritis synovial fibroblasts stimulated with TNF-alpha

Project description:To investigate effects of GLI1, GLI3, and GLI1/3 knockdown on rhematoid arthritis synovial fibroblasts (RASFs) stimulated with TNF-alpha, we pre-treated RASFs (n = 3) with siControl (siCtrl) or siGLI1, siGLI3, or GLI1/3 for 72 hours, and then treated them with TNF-alpha (10 ng/mL) for 24 hours and conducted RNA-seq analysis.

2026-06-10 | GSE329806 | GEO

Transcription profiling of mouse pancreatic islets from wild type and DcR3 transgenic mice to investigate primary non-function (PNF) in islet transplantation

Project description:The islet primary non-function (PNF) is a serious problem in islet transplantation. In this study, we investigated whether DcR3-secreting transgenic (Tg) islets could reduce PNF. We generated transgenic mice expressing human DcR3. The transgenically expressed DcR3 protected islets from IFN-gama plus IL-1beta, or TNF-alpha plus IL-1beta-induced dysfunction and apoptosis in vitro. The Tg islets presented significantly reduced PNF after transplantation. <br><br> Three independent batches of islet isolation were carried out. For each batch, islets were obtained from 4 Tg and 4 WT mice, and pooled respectively. The pooled islets (Tg or WT) were then divided into 4 groups: 2 were cultured in the presence of IFN-gamma (0.5 ug/ml) plus IL-1beta (0.5 ng/ml) with 1 harvested at 24 h and 1 harvested at 48 h; 2 were cultured in the presence of TNF-alpha (100 ng/ml) plus IL-1beta (0.5 ng/ml) with 1 harvested at 24 h and 1 harvested at 48 h. Each treatment employed 3 chips using RNA from 3 different batches of islet isolation. For each treatment, genes with a mean signal strength difference above 2-fold between Tg and WT islets were selected for reverse PCR confirmation.

2009-08-15 | E-MEXP-2306 | biostudies-arrayexpress

Pla2g6-dependent cytokine signaling in MIN6 cells

Project description:Analysis of MIN6 murine beta cell line transfected with Pla2g6 RNAi and treated with pro-inflammatory cytokines TNF-alpha, IL-1beta and IFN-gamma.

2024-02-08 | PXD017863 | Pride

ARH3-regulated cytokine signaling in MIN6 cells

Project description:Analysis of MIN6 murine beta cell line transfected with ARH3 RNAi and treated with pro-inflammatory cytokines TNF-alpha, IL-1beta and IFN-gamma.

2024-05-21 | PXD021501 | Pride

HSP27 3A vs WT

Project description:human bronchial smooth muscle cells were infected with adenoviral constructs containing either the phosphorylation mutant form of HSP27 (HSP27-3A) or the wild type form (HSP27-WT) at 40 MOI for 4 days. All sets were stimulated with a cytokine mixture containing 10 ng/ml IL-1beta, TNF-alfa, and gamma-IFN for 20 hours prior to harvest. This series represents 4 separate preparations of cells and RNA, with each set being subjected to a dye flip and hybridized to 2 different slides. Keywords: parallel sample

2004-04-09 | GSE1292 | GEO

Project description:The human AA dataset 5 includes the gene expression profile of monocyte-derived macrophages isolated from blood donor buffy coats and plated on TCP in medium containing 10% autologous serum. Cells were stimulated for 120 hours with 50 ng/ml of IL-4, 50 U/ml of IFN-γ plus 12.5 ng/ml of TNF-α, 50 ng/ml of M-CSF or 50 ng/ml of IL-10. RNA samples were isolated using TriPure isolation reagent (Roche) and the RNeasy Mini Kit-Qiagen Clean up method. The transcriptional profile was evaluated in two independent cell preparations, each derived from a different single donor using the HT12 V4 R2 bead chip arrays from Illumina.

2013-07-26 | GSE49240 | GEO

Increased Cell Surface Fas Expression is Necessary to Sensitize Lung Fibroblasts to Fas Ligation-Induced Apoptosis: Implications for Fibroblast Accumulation in Idiopathic Pulmonary Fibrosis.

Project description:Idiopathic pulmonary fibrosis (IPF) is associated with the accumulation of collagen-secreting fibroblasts and myofibroblasts in the lung parenchyma. Many mechanisms contribute to their accumulation, including resistance to apoptosis. In previous work, we showed that exposure to the pro-inflammatory cytokines, TNF-α and IFN-γ reverses fibroblast resistance to apoptosis. The goal of this study was to investigate the underlying mechanism. Based on an initial interrogation of the transcriptomes of unstimulated and TNF-α and IFN-γ-stimulated primary lung fibroblasts and the lung fibroblast cell line, MRC5, we show here that among Fas-signaling pathway molecules, Fas expression was increased ~6-fold in an NF-κB and p38mapk-dependent fashion. Prevention of the increase in Fas expression using Fas siRNAs blocked the ability of TNF-α and IFN-γ to sensitize fibroblasts to Fas ligation induced-apoptosis; while enforced adenovirus-mediated Fas overexpression was sufficient to overcome basal resistance to Fas-induced apoptosis. Examination of lung tissues from IPF patients revealed low to absent staining of Fas in fibroblastic cells of fibroblast foci. Collectively, these findings suggest that increased expression of Fas is necessary and sufficient to overcome the resistance of lung fibroblasts to Fas-induced apoptosis. They also suggest that approaches aimed at increasing Fas expression by lung fibroblasts and myofibroblasts may be therapeutically relevant. To investigate the mechanism by which TNF-α and IFN-γ reprogram fibroblasts from resistance to sensitivity to Fas-ligation-induce apoptosis, we exposed human primary lung fibroblasts from an IPF patient (FS087) and non-disease control subject (N78) and the human fetal lung fibroblast cell lung (MRC-5) to TNF-α (10 ng/ml) and IFN-γ (50 U/ml) for 36 hr and analyzed changes in their transcriptomes using Affymetrix microarrays.

2011-01-13 | E-GEOD-26594 | biostudies-arrayexpress

HSP27 3A vs WT

2010-06-09 | E-GEOD-1292 | biostudies-arrayexpress

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).

2010-12-01 | E-GEOD-20297 | biostudies-arrayexpress