Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA167089 | ENA |
REPOSITORIES: ENA
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Project description:Transformed human esophageal keratinocyte cell line EPC2-T (EPC2-hTERT-EGFR-cyclin D1-p53R175H) cells were stimulated with or without 2.5 ng/ml recombinant human TGF-beta1 for 10 days. The above cells were subjected to treatment for 10 days with or without 0.5 µg/ml doxycycline (DOX) to activate tetracycline-inducible (tet-on) ICN1, an active form of Notch1.
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Project description:Senescence, a persistent form of cell cycle arrest, is often associated with a diverse secretome, which provides complex downstream functionality for senescent cells within the tissue microenvironment. We show that oncogene-induced senescence (OIS) is accompanied by a dynamic fluctuation of NOTCH1 activity, which drives a TGF-β-rich secretome, whilst suppressing the senescence-associated pro-inflammatory secretome through inhibition of C/EBPβ. NOTCH1 and NOTCH1-driven TGF-β contribute to ‘lateral induction of senescence’ through a juxtacrine NOTCH-JAG1 pathway. In addition, NOTCH1 inhibition during senescence facilitates upregulation of pro-inflammatory cytokines, promoting lymphocyte recruitment and senescence surveillance in vivo. Because enforced activation of NOTCH1 signalling confers a near mutually exclusive secretory profile compared to typical senescence, our data collectively indicate that the dynamic alteration of NOTCH1 activity during senescence dictates a functional balance between these two distinct secretomes: one representing TGF-β and the other pro-inflammatory cytokines, highlighting that NOTCH1 is a temporospatial controller of secretome composition.
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Project description:NOTCH3 knockdown in non-transformed human esophageal cells
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Project description:For chondrogenic studies of optogenetically activated TGF-β signaling, optogenetic human iPSC-derived MSCs were encapsulated in hydrogels (20 million cells/mL of 2% agarose hydrogel). Groups received either no soluble TGF-β or optogenetic stimulation, or soluble TGF-β3 alone, or optogenetic stimulation alone. After 21 days of differentiation, we performed global quantitative proteomics on samples from two independent experiments, with n=3 replicates per group.
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Project description:TGF-beta plays multiple functions in a board range of cellular responses such as proliferation, differentiation, motility and survival by activating several cellular signaling pathways, including Smads and MAP kinases (Erk, JNK and p38). In particular, TGF-beta can activate pro- or anti-apoptotic signals depending on the target cells. We found that blockage of JNK activation sensitized mouse B lymphoma derived A20 cells to TGF-beta-induced apoptosis. These results suggest that TGF-beta activate JNK to inhibit the activation of death signal that is simultaneously activated by TGF-beta. We used microarrays to gain insight into the effects of JNK inhibition on gene expression in TGF-b-stimulated A20 cells and identified JNK-dependent TGF-beta inducible genes. Experiment Overall Design: The following six samples were prepared: untreated A20 cells (non-stimulated, DMSO): A20 cells cultured with SP600125 for 24 h (non-stimulated, SP600125): A20 cells stimulated with TGF-beta for 12 h (TGF-beta 12 h, DMSO) and 24 h (TGF-beta 24 h, DMSO): and A20 cells stimulated with TGF-beta in the presence of SP600125 for 12 h (TGF-beta 12 h, SP600125) and 24 h (TGF-beta 24 h, SP600125), respectively. Total RNA was prepared and hybridized to the Affymetrix Mouse Genome 430 2.0 array. Genes whose expression was increased by more than 2-fold at either 12 or 24 h after TGF-beta stimulation were identified as TGF-beta inducible genes. Amongst them, we identified genes whose induction levels were reduced by more than 75% by co-treatment with the JNK inhibitor SP600125.
2008-06-15 | E-GEOD-7503 | biostudies-arrayexpress
Project description:This model is from the article:
Quantitative analysis of transient and sustained transforming growth factor-β signaling dynamics.
Zhike Zi, Zipei Feng, Douglas A Chapnick, Markus Dahl, Difan Deng, Edda Klipp, Aristidis Moustakas & Xuedong Liu Molecular Systems Biology
2011 May 24;7:492. 21613981
,
Abstract:
Mammalian cells can decode the concentration of extracellular transforming growth factor-β (TGF-β) and transduce this cue into appropriate cell fate decisions. How variable TGF-β ligand doses quantitatively control intracellular signaling dynamics and how continuous ligand doses are translated into discontinuous cellular fate decisions remain poorly understood. Using a combined experimental and mathematical modeling approach, we discovered that cells respond differently to continuous and pulsating TGF-β stimulation. The TGF-β pathway elicits a transient signaling response to a single pulse of TGF-β stimulation, whereas it is capable of integrating repeated pulses of ligand stimulation at short time interval, resulting in sustained phospho-Smad2 and transcriptional responses. Additionally, the TGF-β pathway displays different sensitivities to ligand doses at different time scales. While ligand-induced short-term Smad2 phosphorylation is graded, long-term Smad2 phosphorylation is switch-like to a small change in TGF-β levels. Correspondingly, the short-term Smad7 gene expression is graded, while long-term PAI-1 gene expression is switch-like, as is the long-term growth inhibitory response. Our results suggest that long-term switch-like signaling responses in the TGF-β pathway might be critical for cell fate determination.
Note:
Developer of the model: Zhike Zi
Reference: Zi Z. et al., Quantitative Analysis of Transient and Sustained Transforming Growth Factor-beta Signaling Dynamics, Molecular Systems Biology, 2011
1. The global parameter that set the type of stimulation
(a) for sustained TGF-beta stimulation: set stimulation_type = 1.
(b) for single pulse of TGF-beta stimulation: set stimulation_type = 2.
parameter "single_pulse_duration" is for the duration of stimulation, for example,
single_pulse_duration = 0.5, for 0.5 min (30 seconds) of TGF-beta stimulation.
*Note: make sure that the time course cover the time point when the event is triggered.
(c) for single pulse of TGF-beta stimulation in COPASI
change the trigger of event "single_pulse_TGF_beta_washout"
from
"and(eq(stimulation_type, 2), eq(time, single_pulse_duration))" (for SBML-SAT)
to
"and(eq(stimulation_type, 2), gt(time, single_pulse_duration))" (for COPASI)
2. Notes for TGF-beta dose in terms of molecules per cell
(a) The following equation applies for conversion of TGF-beta dose in molecules per cell
TGF_beta_dose_mol_per_cell = initial TGF_beta_ex*1e-9*Vmed*6e23
(b) for standard experimental setup 1e6 cells in 2 mL medium
0.001 nM initial TGF_beta_ex is approximately equal to the dose of 1200 TGF-beta molecules/cell
0.050 nM initial TGF_beta_ex is approximately equal to the dose of 60000 TGF-beta molecules/cell
(c) For 1e6 cells in 10 mL medium, please change the initial compartment size of Vmed and the corresponding assignment rule for Vmed.
initial Vmed = 1e-8 (1e6 cells in 10 mL medium)
Vmed = 0.010/(1e6*exp(log(1.45)*time/1440)) (1e6 cells in 10 mL medium)
3. Please note that this model contains events and the medium compartment size is varied.
4. For the model simulation in SBML-SAT, please remove initialAssignments and save it as SBML Level 2 Verion 1 file.
2024-09-02 | BIOMD0000000342 | BioModels
Project description:To identify differentially expressed long noncoding RNAs (lncRNAs) upon TGF-β stimulation in human cultured tubular epithelial cells HK2 and HKC8, we have employed long noncoding RNA microarray expression profiling as a discovery platform to find differentially expressed lncRNAs with TGF-β stimulation in these cells. Cultured human tubular epithelial cells HK2 and HKC8 were stimulated with PBS or TGF-β1. After incubation with TGF-β1 (10ng/ml) for 24 hours, 86 overlapping lncRNAs were upregulated and 47 overlapping lncRNAs were downregulated more than 2 fold vesus cells treated with PBS in these two epithelial cell lines. Expression of ENST00000429588 from this result was quantified in the same RNA samples by real-time PCR, confirming the upregulation upon TGF-β stimulation is repeatable.
2018-08-15 | GSE108554 | GEO
Project description:Transforming growth factor-beta (TGF-β) is a pleiotropic cytokine that dictates T-cell fates in various settings. Despite a wealth of data implicating TGF-β in the differentiation and homeostasis of both suppressive and inflammatory T cells, little is known about the role of TGF-β signaling in the development of memory T cells. This experiment was to correlate gene expression with the finding that TGF-β exposure during human T-cell stimulation ex vivo leads to the accumulation of T cells with central memory (tcm) markers.
2019-07-05 | GSE87508 | GEO
Project description:Mesenchymal stromal cells (MSC) were isolated from human bone marrow. Here, we have compared gene expression profiles of MSC at early and late passages and upon stimulation with transforming growth factor beta 1 (TGF-b1). Stimulation was performed with 1ng/mL TGF-b1 for 1, 4, or 12 hours as indicated. The goal of this study was to determine if senescence-associated gene expression changes and TGF-b1 induced gene expression changes are related. 24 samples were hybridized GeneChip Human Gene 1.0 ST Arrays (Affymetrix)
2014-02-05 | E-GEOD-46019 | biostudies-arrayexpress