Effect of pirfenidone on serum-stimulated human lung fibroblasts
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ABSTRACT:
PROVIDER: PRJNA939233 | ENA |
REPOSITORIES: ENA
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Project description:Idiopathic pulmonary fibrosis (IPF) is an incurable lung disease with a poor prognosis. Fibroblasts and myofibroblasts are the key cells in the fibrotic process. Pirfenidone was approved as an anti-fibrotic drug for IPF treatment as it is able to slow disease progression. The mechanisms by which the drug acts on fibroblasts are not clear. Therefore, this study aims to examine the effects of pirfenidone on the human lung fibroblast (HLF) transcriptome in vitro.
2023-05-12 | GSE226249 | GEO
Project description:Idiopathic Pulmonary Fibrosis (IPF) is a progressive chronic lung disease characterized by excess deposition of extracellular matrix (ECM) proteins in the lung. TGFα is a is a ligand for the epidermal growth factor receptor, and found elevated in several fibrotic lung diseases including IPF. Notably, lung-specific overexpression of TGFα alone in adult mice can cause progressive and extensive adventitial and subpleural fibrosis similar to IPF. Pirfenidone, an FDA approved drug has been shown to improve the decline in lung function in IPF patients. However, the mechanism of action of pirfenidone largely unknown. In the current study, we investigated the effects of pirfenidone using a mouse model of TGFα-induced pulmonary fibrosis and fibroblasts isolated from IPF lungs. Total lung transcriptome analysis suggest a significant overlap in dysregulated gene transcripts between TGFα model and IPF. In vivo studies demonstrate a significant improvement in lung function with pirfenidone therapy compared to vehicle-treated TGFα mice on Dox for six wks. However, pirfenidone treatment did not affect fibroproliferation, myofibroblast transformation, and ECM deposition during TGFα-induced pulmonary fibrosis. In summary, pirfenidone treatment improved lung function but had a limited or no effect on the expression of collagen, ECM genes, fibroproliferation and migration of lung-resident fibroblasts.
2022-06-01 | GSE199034 | GEO
Project description:Investigating the effect of Pirfenidone on NSCLC cells Although immune checkpoint and targeted therapies offer remarkable benefits for lung cancer treatment, some patients do not qualify for these regimens or do not exhibit consistent benefit. Provided that lung cancer appears to be driven by transforming growth factor beta signaling, we investigated the single drug potency of Pirfenidone, an approved drug for the treatment of lung fibrosis which is known to inhibit TGFB1 mRNA. Human A549 and H1975 lung adenocarcinoma cell lines were stimulated for 6h and 25h with 0.75 mg/ml or 1.5 mg/ml Pirfenidone or the respective volume of PBS as vehicle control. Total RNA was extracted and subjected to transcriptome analysis by microarrays.
2019-12-17 | GSE136934 | GEO
Project description:Investigating the effect of Pirfenidone on NSCLC cells Although immune checkpoint and targeted therapies offer remarkable benefits for lung cancer treatment, some patients do not qualify for these regimens or do not exhibit consistent benefit. Provided that lung cancer appears to be driven by transforming growth factor beta signaling, we investigated the single drug potency of Pirfenidone, an approved drug for the treatment of lung fibrosis which is known to inhibit TGFB1 mRNA. Human A549 and H1975 lung adenocarcinoma cell lines were stimulated for 6h and 25h with 0.75 mg/ml or 1.5 mg/ml Pirfenidone or the respective volume of PBS as vehicle control. Total RNA was extracted and subjected to transcriptome analysis by microarrays.
2019-12-17 | GSE136933 | GEO
Project description:Investigating the effect of Pirfenidone on NSCLC cells Although immune checkpoint and targeted therapies offer remarkable benefits for lung cancer treatment, some patients do not qualify for these regimens or do not exhibit consistent benefit. Provided that lung cancer appears to be driven by transforming growth factor beta signaling, we investigated the single drug potency of Pirfenidone, an approved drug for the treatment of lung fibrosis which is known to inhibit TGFB1 mRNA. Human A549 and H1975 lung adenocarcinoma cell lines were stimulated for 6h and 25h with 0.75 mg/ml or 1.5 mg/ml Pirfenidone or the respective volume of PBS as vehicle control. Total RNA was extracted and subjected to transcriptome analysis by microarrays.
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Project description:Serum was added to fibroblasts, and samples were taken.
2013-01-30 | E-SMDB-18 | biostudies-arrayexpress
Project description:Effect of Pirfenidone on NSCLC
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Project description:Serum was added to fibroblasts in the presence of cycloheximide.
2005-01-01 | E-SMDB-19 | biostudies-arrayexpress
Project description:Expression data of stimulated murine primary lung fibroblasts
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Project description:Analysis of platelet-derived growth factor (PDGF)-stimulated fibroblasts. Results provide insight into novel pro-tumorigenic factors induced by PDGF-activation of fibroblasts. 1.2 x 10e6 BJ-hTERT fibroblasts were cultured in 10cm dish with Dulbecco's Modified Eagle Medium (DMEM; Gibco Life Technologies, Gergy-Pontoise, France) containing 1% heat-inactivated fetal calf serum (FCS), 2 mM L-glutamine, penicillin (100 units/ml) and streptomycin (100 ng/ml) at 37ºC in a 5% CO2 humidified atmosphere during 24h. Cultures were stimulated with or without 20ng/mL PDGF-BB (Peprotech, New Jersey, USA) for another 24h prior to harvest. Unstimulated fibroblasts were used as control samples. Cultures of both unstimulated and stimulated fibroblasts were done in triplicate.
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