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Transcriptome analysis after knockdown of target genes (either HSP27 or TGF-β1, both HSP27 and TGF-β1) via shRNAs in SNU-398 cells

ABSTRACT: Transcriptome analysis after knockdown of target genes (either HSP27 or TGF-β1, both HSP27 and TGF-β1) via shRNAs in SNU-398 cells

PROVIDER: PRJNA804180 | ENA |

REPOSITORIES: ENA

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Transcriptome analysis after knockdown of target genes (either HSP27 or TGF-β1, both HSP27 and TGF-β1) via shRNAs in SNU-398 cells

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Transcriptome analysis after knockdown of target genes (either HSP27 or TGF-β1, both HSP27 and TGF-β1) via shRNAs in A549 cells

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Transcriptomic Changes in TGF-β1 Differentiated and PGE2 Dedifferentiated Myofibroblasts

Project description:These data show that the genes that distinguish myofibroblasts from fibroblasts are myriad, and that some genes not traditionally associated with myofibroblast differentiation may serve as novel therapeutic targets for fibrosing disorders. Gene expression levels were assessed from total RNA on the Affymetrix U219 microarray. Here, we use transforming growth factor-β1 (TGF-β1) and prostaglandin E2 (PGE2), which has recently been shown to reverse myofibroblast differentiation, to investigate the transcriptomic changes that occur during TGF-β1-induced differentiation and PGE2-induced de-differentiation of myofibroblasts.

2015-06-30 | E-GEOD-63659 | biostudies-arrayexpress

Transcriptome analysis after knockdown of target genes (either HSP27 or TGF-β1, both HSP27 and TGF-β1) via shRNAs in A549 cells

Project description:Comparing expression profiles : among comparable samples in which target genes are knocked down Global gene expression profiling has shown that more than 1500 (3.2%) genes over 2-fold gene fluctuations are differentially expressed in shTGF-β1-treated cells compared to control shRNA-treated cells.

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Genome-wide transcript profiling for native porcine valvular interstitial cells and those cultured on TCPS and treated with TGF-β1

Project description:Fibrotic diseases have significant health impact and have been associated with differentiation of the resident fibroblasts into myofibroblasts. In particular, stiffened extracellular matrix and TGF-β1 in fibrotic lesions have been shown to promote pathogenic myofibroblast activation and progression of fibrosis in various tissues. To better understand the roles of mechanical and chemical cues on myofibroblast differentiation and how they may crosstalk, we cultured primary valvular interstitial cells (VICs) isolated from porcine aortic valves and studied how traditional TCPS culture, which presents a non-physiologically stiff environment, and TGF-β1 affect native VIC phenotypes. We carried out gene expression profiling using porcine genome microarrays from Affymetrix and found that traditional TCPS culture induces major changes in gene expression of native VICs, rendering these cells more activated and similar to cells treated with TGF-β1. We also monitored time-dependent effects induced by TGF-β1 by examining gene expression changes induced by TGF-β1 at 8 hours and 24 hours. Porcine aortic VICs were isolated and cultured with or without TGF-β1 treatment for RNA extraction and hybridization on Affymetrix microarrays. We included 3 biological replicates for each condition. P0 VICs were freshly isolated cells which had not been cultured. P2 VICs were cells that had been passaged 2 times and cultured on plastic plates in low serum media. Some of the P2 VICs were treated with TGF-β1 at 5ng/ml for 8 hours or 24 hours. All the control and TGF-β1-treated conditions were collected at the same time on day 3 of culture.

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Gene expression profiling in hepatocellular carcinoma cell lines PRC/PRF/5 and SNU-449 after a treatment with Transforming Growth Factor beta (TGF-beta) and Galunisertib, alone or in combination

Project description:Transforming Growth Factor beta (TGF-beta) is a pleiotropic cytokine playing a key role in liver carcinogenesis. The goal of this study was to identify genes differentially expressed in hepatocellular carcinoma cell lines PRC/PRF/5 and SNU-449 after a treatment with TGF-beta and/or Galunisertib, an inhibitor of the type I TGF-beta receptor (TGFBRI). Thus, cells were treated for 16 hours with 1 ng/mL recombinant human TGF-β1 (R&D Systems, Minneapolis, MN) and/or 10 μM LY2157299 (Sigma-Aldrich, St. Louis, MO) after overnight serum starvation. Gene expression profiling was performed using Agilent SurePrint G3 Human GE 8x60K microarrays.

2023-06-01 | GSE211806 | GEO

TGF-β1 activates neutrophil signaling and transcription but not migration

Project description:Tumor-associated neutrophils are found in many types of cancer and are often reported to contribute to negative outcomes. Several studies have shown that the presence of TGF-β in the tumor microenvironment contributes to the skewing of neutrophils to have a more pro-tumor phenotype. However, the direct effects of TGF-β on neutrophil signaling and migration are unclear. We sought to characterize TGF-β signaling in both primary human neutrophils and the neutrophil-like cell line HL-60 and determine whether TGF-β directly induces neutrophil migration. We found that TGF-β1 does not induce neutrophil migration in either a transwell or an underagarose migration assay. However, TGF-β1 does activate signals canonically through SMAD3 and noncanonically through ERK1/2 in neutrophils in a time and dose-dependent manner. Additionally, TGF-β1 present in the tumor-conditioned media (TCM) is responsible for SMAD3 activation. Moreover, we discovered that TCM from aggressive breast cancer cells induces neutrophils to secrete leukotriene B4 (LTB4), which is a lipid mediator important for amplifying neutrophil recruitment. However, we found that TGF-β1 alone does not induce secretion of LTB4. We next performed RNA-sequencing to evaluate the effects of TGF-β1 and TCM on the neutrophil transcriptome. We found that TGF-β1 and TCM result in changes in gene transcription in HL-60 cells, specifically of two pro-tumor genes OSM and VEGFA. Together, our findings characterize the effects of TGF-β1 on neutrophil signaling, migration, and gene expression that can be applied to understanding the changes in neutrophils that occur in the tumor microenvironment.

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A novel non-canonical signaling pathway mediates TGF-β1-induced glucocorticoid insensitivity in epithelial cells

Project description:Limited therapeutic responses to glucocorticoids in chronic inflammatory disease are partly attributable to interleukins and transforming growth factor-β1 (TGF-β1). Global inhibition of TGF-β1 carries known risks, including autoimmune disease. Here we elucidate the signaling pathway subserving modulation of glucocorticoid activity by TGF-β1. The proteomic response of airway epithelial cells to TGF-β1 revealed 24 candidate proteins of which 3 were prioritized by exclusion of changes induced by: TGF-β2, which lacks the modulatory activity of TGF-β1 and TGF-β3; and those of TGF-β1 that were prevented by small molecule inhibitors of non-canonical TGF-β1 signaling, that did not prevent glucocorticoid modulation. Pharmacological and genetic approaches establish that TGF-β1-induced glucocorticoid insensitivity is mediated by a novel signaling cascade involving LIM domain kinase 2 mediated phosphorylation of phospho-cofilin1 that activates phospholipase D to generate the effector(s) (lyso)phophatidic acid. This study identifies several promising drug targets that potentially enable safe modulation of TGF-β1 in chronic inflammatory diseases.

2019-01-27 | GSE104908 | GEO

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