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Transcriptome analysis of lung fibroblasts from 5 control and 5 IPF patients with/out TGF-b1 stimulation

ABSTRACT: Transcriptome analysis of lung fibroblasts from 5 control and 5 IPF patients with/out TGF-b1 stimulation

PROVIDER: PRJNA530261 | ENA |

REPOSITORIES: ENA

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Transcriptome analysis of lung fibroblasts from 5 control and 5 IPF patients with/out TGF-b1 stimulation

Project description:Isolated primary human fibroblasts from 5 control and 5 IPF patients were treated with/out 3ng/ml TGF-b1 for 24 hours before cells were lysed for RNA extraction.

2019-04-02 | GSE129164 | GEO

ChIP-seq analysis of the TGF-b1-treated intestinal organoids with or without Smad4 loss

Project description:The ChIP-seq analysis vilidated that Yap1/Smad2/3 signaling could regulate the transcriptional activity of key inflammasome genes upon TGF-b stimulation. In addition, TGF-b1 could be the downstream target gene of Yap. Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for Yap1, Smad2/3 as well as the Tead1 in indicated intestinal organoids.

2024-06-01 | GSE229996 | GEO

Therapeutic activity of GARP:TGF-b1 blockade in murine primary myelofibrosis

Project description:Primary myelofibrosis (PMF) is a myeloproliferative neoplasm characterized by clonal expansion of myeloid cells, notably megakaryocytes (MKs), and aberrant cytokine production leading to bone marrow (BM) fibrosis and insufficiency. Current treatment options are limited. TGF-b1, a profibrotic and immunosuppressive cytokine, is involved in PMF pathogenesis. While all cell types secrete inactive, latent TGF-b1, only a few activate the cytokine via cell type-specific mechanisms. The cellular source of the active TGF-b1 implicated in PMF is not known. Transmembrane protein GARP binds and activates latent TGF-b1 on the surface of regulatory T lymphocytes (Tregs) and MKs or platelets. Here, we found increased expression of GARP in BM and spleen of mice undergoing PMF and tested the therapeutic potential of a monoclonal antibody that blocks TGF-b1 activation by GARP-expressing cells. GARP:TGF-b1 blockade reduced not only fibrosis, but also clonal expansion of transformed cells. Using mice carrying a genetic deletion of Garp in either Tregs or MKs, we found that the therapeutic effects of GARP:TGF-b1 blockade in PMF imply targeting GARP on Tregs. These therapeutic effects, accompanied by increased IFN-g signals in the spleen, were lost upon CD8 T cell depletion. Our results suggest that selective blockade of TGF-b1 activation by GARP-expressing Tregs increase a CD8 T cell-mediated immune reaction that limits transformed cell expansion, providing a novel approach that could be tested to treat patients with myeloproliferative neoplasms.

2022-10-27 | GSE216221 | GEO

Secretomics of TGF-B1-stimulated IMR-90 cells with and without sanglifehrin A

Project description:Proteins secreted from TGF-B1-stimulated IMR-90 cells with and without sanglifehrin A were profiled.

2024-10-17 | PXD029541 | Pride

Transcription profiling of mouse mammary epithelial cells NMuMG treatd with TGF-b1 - time series experiment

Project description:Response of mouse mammary epithelial cells NMuMG to TGF-b1 - time course experiment. Identification of novel gene targets involved in TGF-b1-driven regulation of epithelial-mesenchymal transition (EMT).

2004-10-01 | E-MEXP-139 | biostudies-arrayexpress

Basonuclin-1 modulates epithelial plasticity and TGF-β1-induced loss of epithelial cell integrity [BNC1]

Project description:TGF-b1-stimulation induces an epithelial dedifferentiation-process, throughout which epithelial cell sheets disintegrate and gradually switch into fibroblastic-appearing cells (EMT-like transition). Several transcription factors, some of them being TGF-b1-responsive, are functionally involved in such a switch and affect epithelial differentiation and plasticity. We used microarray-based gene expression profiling of mammary epithelial cells that actively undergo TGF-b1-induced epithelial dedifferentiation. Further, we determined gene expression changes in Basonuclin-1 knock-down cells in conjunction with TGF-b1-stimulation in order to determine a possible effect of Bnc1 on TGF-b1-responsive genes.

2014-03-01 | GSE54715 | GEO

Basonuclin-1 modulates epithelial plasticity and TGF-?1-induced loss of epithelial cell integrity [BNC1]

2014-03-01 | E-GEOD-54715 | biostudies-arrayexpress

Cardiac-derived TGF-b1 confers resistance to diet-induced obesity through regulation of adipocyte size and function.

Project description:Regulation of organismal homeostasis in response to nutrient availability is a vital physiological process that involves inter-organ communication. Understanding the mechanisms controlling systemic cross talk for maintenance of metabolic health is critical to counteract diet-induced obesity. Here, we show that cardiac-derived transforming growth factor beta 1 (TGF-b1) protects against weight gain and glucose intolerance in mice subjected to high-fat diet. Secretion of TGF-b1 by cardiomyocytes correlates with bioavailability of this factor in circulation. TGF-b1 prevents adipose tissue inflammation independent of body weight and glucose metabolism phenotypes, suggesting protection from adipocyte dysfunction-driven immune cell recruitment. TGF-b1 alters gene expression programs in white adipocytes, favoring their thermogenic fate and consequently increasing their mitochondrial oxygen consumption rates. Ultimately, subcutaneous and visceral white adipose tissue from heart-specific TGF-b1 transgenic mice fail to undergo cellular hypertrophy, leading to reduced overall adiposity during high-fat feeding. Thus, TGF-b1 is a critical mediator of heart-fat communication for regulation of systemic metabolism.

2021-11-03 | GSE179102 | GEO

Gene expression profile of human peritoneal mesothelial cells (HPMC) treated with TGF-b1

Project description:Long-term peritoneal dialysis is associated with progressive fibrosis of the peritoneum. Epithelial-mesenchymal transition (EMT) of mesothelial cells is an important mechanism involved in peritoneal fibrosis, and TGF-b1 is considered central in this process. We conducted network-based integrated analysis of transcriptomic data to systemically characterize the molecular signature of TGF-b1-stimulated human peritoneal mesothelial cells (HPMCs).

2018-10-18 | GSE121372 | GEO

Comparison of the LIGHT and TGF-B1 induced transcriptomes in esophageal FBL

Project description:To understand the transcriptional responses induced by LIGHT in esophageal fibroblasts and compare them to the pro-fibrotic TGF-B1

2020-08-03 | GSE143482 | GEO

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