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Fig. 5 | Respiratory Research

Fig. 5

From: IL-1β augments TGF-β inducing epithelial-mesenchymal transition of epithelial cells and associates with poor pulmonary function improvement in neutrophilic asthmatics

Fig. 5

The candidate signaling pathways mediated the process of IL-1β augmenting TGF-β1-induced EMT in A549 cells. A549 cells were cultured in the absence (−) or presence (+) of TGF-β1, IL-1β. a Proteomic analyses of p-ERK1/2, p-JNK1/2, p-p38, p-AKT, p-NFκB, and p-smad3. The relative b p-ERK1/2, c p-JNK1/2, and d p-p38 protein expression were assessed by means of western blot. Expression levels were normalized to the housekeeping gene GAPDH and calculated over untreated control cells. Then the inhibitors of e MEK, f p-JNK1/2, and g p-p38 were used to determine if the process of IL-1β augmenting TGF-β1-induced EMT in A549 cells was mediated by MAPK signaling pathways. A549 cells were cultured in the absence (−) or presence (+) of TGF-β1, IL-1β, and three inhibitors of MAPK signaling pathway. The protein expressions of E-cadherin and Fibronectin were assessed by western blot analysis. The figures bd illustrate cumulative data from 3 independent experiments. Error bars represent standard deviation. *p < 0.05, **p < 0.01, ***p < 0.001 compared with control group. #p < 0.05, ##p < 0.01, ###p < 0.001 compared with TGF-β1 treated group

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