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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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			Action	DRS
	SRR26187164_1.fastq.gz	Fastqsanger.gz
	SRR26187164_2.fastq.gz	Fastqsanger.gz
	SRR26187165_1.fastq.gz	Fastqsanger.gz
	SRR26187165_2.fastq.gz	Fastqsanger.gz
	SRR26187166_1.fastq.gz	Fastqsanger.gz

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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

RNAseq analysis of Campylobacter jejuni's response to glutamine addition in growth media

Project description:Campylobacter jejuni is a human pathogen which causes campylobacteriosis, one of the most widespread zoonotic enteric diseases worldwide. Growth of Campylobacter can be improved through the addition of glutamine to media which serves as the nitrogen source. RNAseq was used to identify the transcriptomic response of Campylobacter jejuni when the nitrogen source was switched from serine (poor growth) to glutamine (good growth) in chemostat cultures.

2022-12-01 | E-MTAB-11495 | biostudies-arrayexpress

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Project description:To understand the effects of glutamine deprivation on cell physiology we performed global analysis of gene expression in response to glutamine deprivation. U2OS cells were subjected to glutamine deprivation for 24h followed by RNA extraction and microarray analysis. U2OS cells were plated overnight followed by treatment for 24h with glutamine-containing and glutamine-depleted media. Three biological replicates were assayed for each condition.

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MCF7 cells exposed to conditioned media from growing or senescent fibroblasts

Project description:MCF7 cells exposed to conditioned media from growing or senescent fibroblasts

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Project description:RNAseq analysis of Campylobacter jejuni's response to glutamine addition in growth media

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Project description:Dynamic mRNA gene expression from the wildtype YSBN6 during a nutritional downshift from glutamine to proline. Glutamine and proline were initially together in the media, with cells consuming exlusively glutamine (proline utilization inhibited due to nitrogen catabolite repression). The concentration of glutamine was frequently evaluated at-line, and the moment at which glutamine was not detected anymore is referred to as the time of the shift.

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

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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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