RNA-seq in Hs578T cells stimulated with TGF-β
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ABSTRACT:
PROVIDER: PRJNA639269 | ENA |
REPOSITORIES: ENA
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Project description:The goal of the study was to identify the effects of TGF-beta on primary human macrophages maturated under different conditions. Experiment Overall Design: For the analysis of TGF-beta effects macrophages were differentiated in the presence of IL-4 or IL-4 in combination with dexamethasone. After 5 days differentiation mature macrophages were stimulated by TGF-beta for 24 hours. In the case of IL-4/dexamethasone stimulation an additional data point was taken. In this case macrophages were also stimulated by TGF-beta for 3 hours. For every group 5 independent donors were taken.
2008-06-20 | E-GEOD-7568 | biostudies-arrayexpress
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:Background and Aims: Transforming growth factor (TGF-β) induced activation of quiescent hepatic stellate cells (HSC) and their transformation to myofibroblasts is a key event in liver fibrosis and portal hypertension. GIPC (also referred to as synectin) is a downstream signal activation molecule of TGF-β and other receptors. In this study, we sought to identify novel genes targeted by TGF-β and GIPC and elucidate if and how they may contribute to liver fibrosis. Methods and Results: We performed sequential mRNA sequencing analysis on TGF-β stimulated HSC and then on TGF-β-stimulated HSC in presence and absence of GIPC knockdown. IGFBP-3, an insulin growth factor transport protein, emerged as a top activation target of both TGF-β and GIPC, which was confirmed by qPCR, ELISA and Western blot (WB) analysis. Targeted chromatin immunoprecipitation (ChIP) revealed that GIPC increases the histone 3 lysine 27 (H3K27) acetylation activating mark and concurrently decreases the H3K27 inhibitory trimethylation (H3K27m3) mark providing an epigenetic correlate to the gene regulation changes. In vivo, global knockout of IGFBP-3 mice resulted in attenuation of HSC activation markers and attenuation of portal pressure in response to chronic liver injury models. Analysis of serum levels from cirrhotic patients also showed IGFBP-3 increase of more than 2-fold compared to healthy controls. Finally, in vitro mechanism studies revealed that IGFBP-3 promotes HSC migration through integrin dependent phosphorylation of AKT. Conclusion: TGF-β upregulates IGFBP-3 through GIPC leading to increased HSC migration in vitro and promotes portal hypertension in vivo. These studies support the role of IGFBP-3 as a potential pathophysiologic target or biomarker in chronic liver disease.
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