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• W2008493932 abstract "BackgroundCCAAT/enhancer-binding proteins (C/EBPs) control cell proliferation; lack of C/EBPα correlates with increased proliferation of bronchial smooth muscle cells (BSMCs) of asthmatic patients.ObjectiveWe sought to assess disease-specific expression of C/EBPα, β, δ, and ε and the effects of budesonide (10−8 mol/L) and formoterol (10−8 mol/L).MethodsExpression and function of C/EBPα, β, δ, and ε BSMCs of control subjects (n = 9), asthmatic patients (n = 12), and patients with chronic obstructive pulmonary disease (COPD; n = 10) were determined.ResultsThe control group expressed C/EBPα, β, δ, and ε, which were upregulated by serum (5%). Budesonide completely inhibited C/EBPα and β expression; formoterol increased C/EBPα expression (2-fold). C/EBPδ and ε expression were not affected by the drugs. The asthmatic group did not appropriately express C/EBPα. Basal levels of C/EBPβ, δ, and ε were upregulated by serum (5%). Budesonide and formoterol increased C/EBPβ levels (3.4-fold and 2.5-fold, respectively), leaving C/EBPα, δ, and ε levels unaffected. The COPD group normally expressed C/EBPα, β, and ε, which were upregulated by serum treatment (5%). Basal levels of C/EBPδ were downregulated by serum in 7 of 10 BSMC lines. Budesonide inhibited C/EBPα and β expression, upregulated C/EBPδ (3.2-fold), and had no effect on C/EBPε. Formoterol upregulated C/EBPα expression (3-fold) but not the other C/EBPs. Protein analysis and electrophoretic mobility shift assay confirmed the disease-specific expression pattern of C/EBPα in asthmatic patients and C/EBPδ in patients with COPD.ConclusionsThe expression and regulation of C/EBPs in BSMCs of asthmatic patients and patients with COPD seems disease specific. Budesonide and formoterol modulate C/EBP expression in a drug- and disease-specific pattern.Clinical implicationsThe data could provide a method to discriminate between asthma and COPD at an early disease stage. CCAAT/enhancer-binding proteins (C/EBPs) control cell proliferation; lack of C/EBPα correlates with increased proliferation of bronchial smooth muscle cells (BSMCs) of asthmatic patients. We sought to assess disease-specific expression of C/EBPα, β, δ, and ε and the effects of budesonide (10−8 mol/L) and formoterol (10−8 mol/L). Expression and function of C/EBPα, β, δ, and ε BSMCs of control subjects (n = 9), asthmatic patients (n = 12), and patients with chronic obstructive pulmonary disease (COPD; n = 10) were determined. The control group expressed C/EBPα, β, δ, and ε, which were upregulated by serum (5%). Budesonide completely inhibited C/EBPα and β expression; formoterol increased C/EBPα expression (2-fold). C/EBPδ and ε expression were not affected by the drugs. The asthmatic group did not appropriately express C/EBPα. Basal levels of C/EBPβ, δ, and ε were upregulated by serum (5%). Budesonide and formoterol increased C/EBPβ levels (3.4-fold and 2.5-fold, respectively), leaving C/EBPα, δ, and ε levels unaffected. The COPD group normally expressed C/EBPα, β, and ε, which were upregulated by serum treatment (5%). Basal levels of C/EBPδ were downregulated by serum in 7 of 10 BSMC lines. Budesonide inhibited C/EBPα and β expression, upregulated C/EBPδ (3.2-fold), and had no effect on C/EBPε. Formoterol upregulated C/EBPα expression (3-fold) but not the other C/EBPs. Protein analysis and electrophoretic mobility shift assay confirmed the disease-specific expression pattern of C/EBPα in asthmatic patients and C/EBPδ in patients with COPD. The expression and regulation of C/EBPs in BSMCs of asthmatic patients and patients with COPD seems disease specific. Budesonide and formoterol modulate C/EBP expression in a drug- and disease-specific pattern." @default.
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• W2008493932 date "2007-01-01" @default.
• W2008493932 modified "2023-10-10" @default.
• W2008493932 title "Disease-specific expression and regulation of CCAAT/enhancer-binding proteins in asthma and chronic obstructive pulmonary disease" @default.
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• W2008493932 doi "https://doi.org/10.1016/j.jaci.2006.07.056" @default.
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