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Transcriptome profiling of control cells or the A549 cells in the presence or absence of acetate following TGF-β1 stimulation

ABSTRACT: Transcriptome profiling of control cells or the A549 cells in the presence or absence of acetate following TGF-β1 stimulation

PROVIDER: PRJNA809029 | ENA |

REPOSITORIES: ENA

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Transcriptome profiling of control cells or the A549 cells in the presence or absence of acetate following TGF-β1 stimulation

Project description:Purpose: To compare the transcriptome profiling of control cells or the A549 cells in the presence or absence of acetate following TGF-β1 stimulation. Methods: A549 cells were treated with control, TGF-β1 or TGF-β1 plus acetate for 2 days. And then, we performed RNA sequencing for transcription profiling of control cells or the A549 cells in the presence or absence of acetate following TGF-β1 stimulation. The raw data were processed with bcl2fastq software and HISAT2. Results: From the transcriptome profiling and analysis, we got gene expression data of control group and in the presence or absence of acetate following TGF-β1 stimulation using A549 cells. Conclusion: The gene expression data revealed the transcriptome variation by TGF-β1 treatment and acetate can reverse TGF-β1 effect.

2022-06-14 | GSE197132 | GEO

Transcriptomic profiling of MGT#1-mVenus-reporter harboring A549 and H1944 cells upon stimulation with GSK126 and TGF-β1.

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Transcriptome profiling of mouse CD8+ T cells in the presence or absence of acetate

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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.

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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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2022-02-08 | GSE196286 | GEO

Transcriptome profiling of mouse CD4+ T cells in the presence or absence of acetate

Project description:Transcription profiling was performed on mouse CD4+ T cells treated with or without 10 mM acetate for 24 h. We then performed gene expression profiling analysis using data obtained from RNA-seq of mouse CD4+ T cells.

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TGF-β1 induces bone marrow NK cells dysfunction

Project description:TGF-β1 is a cytokine of the bone morphogenetic protein–activin family and commonly regarded as the most powerful immunosuppressive cytokine

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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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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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