Proteomic study of NXDA on TGF-β-induced activation of rat cardiac fibroblasts
Ontology highlight
ABSTRACT:
ORGANISM(S): Rattus Norvegicus
SUBMITTER: 
Yundai Chen
PROVIDER: PXD078180 | iProX | Fri May 08 00:00:00 BST 2026
REPOSITORIES: iProX
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Project description:Primary cardiac fibroblasts were isolated from neonatal C57BL/6J mouse hearts and stimulated with TGF-β1 in vitro to induce a profibrotic phenotype. Bulk RNA sequencing was performed on fibroblasts treated with TGF-β for 48 hours and on matched untreated controls to characterize transcriptional programs associated with TGF-β–driven fibroblast activation. Differential expression and gene ontology analyses were used to identify pathways related to extracellular matrix remodeling, TGF-β signaling, and DNA damage responses. These data support mechanistic studies on CRABP2–MRE11–MRN–dependent regulation of cardiac fibroblast activation and fibrosis.
2026-01-06 | GSE315365 | GEO
Project description:Advanced ovarian cancer is the most lethal gynecologic malignancy in the United States. Ovarian cancer cells are known to have diminished response to TGF-beta, but it remains unclear whether TGF-beta can modulate ovarian cancer cell growth in an indirect manner through cancer-associated fibroblasts (CAFs). Using transcriptome profiling analyses on TGF-beta-treated ovarian fibroblasts, we identified a TGF-beta-responsive gene signature in ovarian fibroblasts. Identifying TGF-beta-regulated genes in the ovarian microenvironment helps in understanding the role of TGF-beta in ovarian cancer progression. The human telomerase-immortalized ovarian fibroblast line NOF151 was treated with 5ng/mL of either TGF-beta-1 or TGF-beta-2. Total RNA was isolated from control samples and TGF-beta-treated fibroblasts samples at 48 hours post-treatment, followed by cDNA synthesis, IVT and biotin labeling. Samples were then hybridized onto Affymetrix Human Genome U133 Plus 2.0 microarrays. For each treatment group, three independent samples were prepared for the microarray experiment.
2013-12-31 | E-GEOD-40266 | biostudies-arrayexpress
Project description:To assess the transcriptomic response of human lung fibroblast to TGF-β, human MRC5 pulmonary fibroblasts (CCL-171) were exposed or not to TGF-β at 10 ng/mL. RNA samples were harvested 24 hours after TGF-β exposition. Three independent experiments were carried out.
2019-04-11 | GSE97829 | GEO
Project description:Myocardial infarctions cause hypoxic injury to downstream tissue and a consequent fibrotic remodeling process to replace injured tissue with a scar. Scar formation occurs through phases of wound healing in which stimuli such as transforming growth factor-beta (TGF-β) drive cardiac fibroblasts to activate into a myofibroblast phenotype and deposit matrix molecules that form a scar. While this is necessary to repair injured tissue, excessive fibrosis commonly occurs which is correlated with heart failure. Therefore, defining cardiac fibroblast phenotypes under hypoxic stimuli and TGF-β is essential for understanding and treating pathological fibrosis. We robustly characterized fibroblast phenotype through immunofluorescence, quantitative RT-PCR, and proteomic analysis, after either TGF-β treatment or hypoxia durations that mimic acute hypoxic injury post-infarction. We find that hypoxic fibroblasts respond to low oxygen with increased hypoxia inducible factor 1 (HIF-1) but not HIF-2 activity by 4h. This is accompanied by increased gene and protein levels of VEGFA and LOX, respectively, which are both targets of HIF-1. Both TGF-β1 and hypoxia inhibit proliferation by 24h. While TGF-β1 treatment upregulated various fibrotic pathways, hypoxia causes a global reduction in protein synthesis, including collagen biosynthesis. This study discerns overlapping from distinctive outcomes of TGF-β1 and hypoxia treatment, which is important for elucidating their roles in fibrotic remodeling post-MI.
2024-07-03 | PXD051197 | Pride
Project description:To assess the transcriptomic response of human lung fibroblast to TGF-β, human MRC5 pulmonary fibroblasts (CCL-171) were exposed to TGF-β at 10 ng/mL. RNA samples were harvested 24 hours after TGF-β exposition. Three independent experiments were carried out.
2019-04-11 | GSE97832 | GEO
Project description:The survival of isolated metastatic cells and expansion into macroscopic tumour has been recognized as a limiting step for metastasis formation in several cancer types yet the determinants of this process remain largely uncharacterized. In colorectal cancer (CRC), we identify a transcriptional programme in tumour-associated stromal cells, which is intimately linked to a high risk of developing recurrent disease after therapy. A large proportion of CRCs display mutational inactivation of the TGF-beta pathway but paradoxically they are characterized by high TGF-beta production. In these tumours, TGF-beta instructs a transcriptional programme in stromal cells, which confers a high risk of developing metastatic disease. We quantified the association of TGF-beta-activated fibroblasts with disease progression. To this end, we used as surrogates the gene expression programme upregulated by addition of TGF-beta to normal colon mucosa-derived fibroblasts (CCD-Co-18) in culture. CCD-Co-18 were seeded at 60% confluence and treated with TGF-β1. Gene expression profiles were measured in duplicate using HG-U133 plus 2.0. We used RMA background correction, quantile normalization and RMA summarization (Gautier et al., 2004). A TGF-β response signature was obtained by selecting genes with limma P-value < 0.05 and at least two fold up-regulation in TGF-β treated fibroblasts.
2013-01-17 | E-GEOD-39394 | biostudies-arrayexpress
Project description:Background: Asthma is the most common chronic lung disease in children and young adults worldwide. Airway remodelling (including increased fibroblasts and myofibroblasts in airway walls due to chronic inflammation) differentiates asthmatic from non-asthmatic airways. The increase in airway fibroblasts and myofibroblasts occurs via epithelial to mesenchymal transition (EMT) where epithelial cells lose their tight junctions and are transdifferentiated to mesenchymal cells, with further increases in myofibroblasts occurring via fibroblast-myofibroblast transition (FMT). Transforming growth factor (TGF)-β is the central EMT- and FMT-inducing cytokine. In this study, we have used next generation sequencing to delineate the changes in the fibroblast transcriptome induced by TGF-β treatment in both the short term and after differentiation into myofibroblasts, to gain an understanding of the contribution of TGF-b induced transdifferentiation to the asthmatic phenotype. The data obtained from RNAseq analysis was confirmed by quantitative PCR (qPCR). Results: As expected, we found that genes coding for intermediates in the TGF-β signalling pathways (SMADs) were differentially expressed after treatment, and genes involved in cytoskeletal pathways (FN1, LAMA, ITGB1) were differentially expressed in myofibroblasts compared to fibroblasts. Importantly, genes that were previously shown to be changed in asthmatic lungs (ADAMTS1, DSP, TIMPs, MMPs) were differentially expressed in myofibroblasts, strongly suggesting that TGF-β mediated differentiation of fibroblasts to myofibroblasts may underlie important changes in the asthmatic airway. We also identified new signalling pathways (AKT, PTEN) that are changed in myofibroblasts compared to fibroblasts. Conclusion: We have found a significant number of genes that are altered after differentiation of fibroblasts into myofibroblasts by TGF-β treatment, many of which were expected or predicted. However, we also identified novel genes and pathways that were affected after treatment of fibroblasts with TGF-β, which suggests additional pathways that that are activated during the transition between fibroblasts and myofibroblasts, and may contribute to the asthma phenotype.
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Project description:Advanced ovarian cancer is the most lethal gynecologic malignancy in the United States. Ovarian cancer cells are known to have diminished response to TGF-beta, but it remains unclear whether TGF-beta can modulate ovarian cancer cell growth in an indirect manner through cancer-associated fibroblasts (CAFs). Using transcriptome profiling analyses on TGF-beta-treated ovarian fibroblasts, we identified a TGF-beta-responsive gene signature in ovarian fibroblasts. Identifying TGF-beta-regulated genes in the ovarian microenvironment helps in understanding the role of TGF-beta in ovarian cancer progression.
2013-12-31 | GSE40266 | GEO
Project description:To assess the role of the lncRNA DNM3OS in TGF-β-induced lung fibroblast activation, we transfected in human MRC5 pulmonary fibroblasts (CCL-171) a gapmer designed against DNM3OS for 48h and then exposed these cells to TGF- β (10 ng/mL). RNA samples were harvested 24 hours after TGF-β exposition. Two independent experiments were carried out.
2019-04-11 | GSE97823 | GEO
Project description:To understand the role of areca nut and TGF-β induced gene expression changes in fibroblasts and its contibution in the manifestation of Oral submucous fibrosis, we studied gene expression profile in primary human gingival fibroblast (hGF) cells following treatment with areca nut, TGF-β and both together. Control Vs Areca nut 5 µg/ml water extract (5H) (2), Contro Vs TGF-β (2), Control Vs Areca nut (5 µg/ml) and TGF-β (5 ng/ml) (5H+T) (2). (2)- Biological duplicates.
2015-07-06 | E-GEOD-59414 | biostudies-arrayexpress