Skip to main content
Fig. 6 | Respiratory Research

Fig. 6

From: Combination of glycopyrronium and indacaterol inhibits carbachol-induced ERK5 signal in fibrotic processes

Fig. 6

GLY and IND suppressed ERK5 phosphorylation in response to CCh or TGF-β1 in lung fibroblasts. Sub-confluent HFL1 cells were cultured in SF-DMEM with or without CCh (a) or TGF-β1 (b) for the indicated times. ERK5 phosphorylation was determined by immunoblotting. The bands with slower electrophoretic mobility corresponded to the activated kinase. Sub-confluent HFL1 cells (c, d) or primary fibroblasts (e-h) were serum deprived for 24 h followed by stimulation with or without TGF-β1 or CCh in the presence or absence of GLY and/or IND, SB431542 and ERK5 inhibitor (BIX02189) for 48 h. Cells were harvested and immunoblotted for ERK5. Each pair of symbols connected by a line represents data from an individual cell strain. Cells from non-smokers are indicated by open circles, cells from patients with COPD (GOLD I) by squares, and cells from patients with COPD (GOLD II) by closed circles. Vertical axis, the fold increase in activated kinase (p-ERK5) against total ERK5 over control or relative intensity of ERK5/β-actin ratio; Horizontal axis, times or conditions. All values represent the mean ± SEM. P < 0.05, compared with solvent control. *P < 0.05, **P < 0.01, compared with stimulus. § P < 0.05, compared with non-smokers and COPD lung fibroblasts in the same stimulus group

Back to article page