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Effect of TGF-B1 on primary human lung fibroblasts growing in media with physiological glucose and glutamine

ABSTRACT: Effect of TGF-B1 on primary human lung fibroblasts growing in media with physiological glucose and glutamine

PROVIDER: PRJNA1021225 | ENA |

REPOSITORIES: ENA

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Effect of TGF-B1 on primary human lung fibroblasts growing in media with physiological glucose and glutamine

Project description:The interplay between metabolism and gene expression is primarily known through epigenetic modifications which use metabolites such as acetyl-CoA. Glucose and glutamine are critical for the synthesis of these metabolites but the concentrations of these two major nutrients are not standardized in conventional tissue culture media. The aim of this study was to investigate the transcriptomic effect of TGF-B1 after 24 hours in primary human lung fibroblasts (pHLFs) growing in DMEM with glucose and glutamine set at physiological concentrations (5 and 0.7 mM, respectively). We were then able to compare these gene expression patterns to a previously published dataset of pHLFs growing in DMEM with higher concentrations of glucose and glutamine (25 and 2 mM, respectively) (GSE102674). This revealed a dramatic difference of roughly 3-fold differentially expressed genes dependent on DMEM formulation as well as just half of the top 20 enriched pathways induced by TGF-B1 shared, as analysed with GSEA. The conclusion was that the concentrations of glucose and glutamine have profound effects on gene expression changes.

2024-09-02 | GSE244098 | GEO

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.

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Dynamic mRNA gene expression during a nutritional upshift from proline to glutamine

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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.

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

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

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Novosphingobium sp. B1 strain:B1

Project description:Novosphingobium sp. B1 strain:B1 Genome sequencing

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

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2018-10-18 | GSE121372 | GEO

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