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- W2309114897 abstract "Introduction: COPD is characterised by chronic airway inflammation resulting in extensive airway remodelling. The origin of the remodelling pathology in COPD is unknown and may result from increased EMT (epithelial-mesenchymal transition). EMT is a process which is mediated by hypoxia and several growths factors, such as transforming growth factor-beta (TGF-β1). Formoterol is a long acting beta2 agonist which can exert antiinflammatory effects by the regulation of intracellular cAMP levels. The aim of our study was to determine if formoterol can modulate down-stream mediators of EMT by cAMP induction.Methods: Human bronchial smooth muscle cell culture was performed using standard protocols.Cells were stimulated with Formoterol (10-10 to -6 M), Dideoxyadenosin (DDA, 100μM), and/or TGF-β1 (5ng/ml); Forskolin was used as a positive control. cAMP measurement was performed by ELISA (at 1, 3 and 6 hours).CTGF, Collagen 1A1 (Col1) and Collagen4 (Col4) mRNA transcription was measured by quantitative real time PCR (18S mRNA served as reference gene). All experiments were performed as triplicates.Results: Formoterol significantly increased intracellular cAMP after 1, 3 and 6 hours compared to untreated cells, whereas the maximum effect was observed after 1 hour. The cAMP increase was effectively blocked by the addition of DDA at any time point. After 24 hours, Formoterol significantly reduced TGF-β1 stimulated Col1 and CTGF but not Col4 mRNA transcription. The addition of DDA reversed this effect for Col1 but not for CTGF.Conclusion: Treatment with formoterol resulted in a decrease of TGF-β1 induced mediators of extracellular matrix composition. These new findings suggest a potential role for formoterol in EMT." @default.
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- W2309114897 date "2011-09-01" @default.
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- W2309114897 title "Effects of formoterol on TGF-β1 induced factors of extracellular matrix composition" @default.
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