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. 2022 Dec 28;23:381. doi: 10.1186/s12931-022-02285-2

Fig. 2.

Fig. 2

Amphiregulin (AREG)-induced cellular communication network factor 2 (CCN2) and fibronectin expressions in A549 human lung epithelial cells. A A549 cells were stimulated with 0 ~ 100 ng/ml AREG for 6 h, and the expression of communication network factor 2 (CCN2) reached its highest level with 10 ng/ml AREG. Cell lysates were prepared and immunodetected with specific antibodies for CCN2 and α-tubulin. Results are expressed as the mean ± SEM, *p < 0.05, n = 3, compared to the group without AREG treatment. B Cells were incubated with AREG (10 ng/ml) for 0 ~ 8 h, and then the CCN2 and α-tubulin proteins were determined by immunoblots. Data are presented as the mean ± SEM of three experiments. *p < 0.05, compared to the control. Cells were treated with AREG (10 ng/ml) for the indicated time interval. E-cadherin and α-tubulin proteins, (C) Fibronectin and α-tubulin proteins (D) were determined by immunoblots. Data are presented as the mean ± SEM of three experiments. *p < 0.05, compared to the control. E Cells were treated with AREG (10 ng/ml) for 0 ~ 24 h, and wound area (yellow square area) was quantified by image J. Data are presented as the mean ± SEM, n = 3. *p < 0.05, compared to the control. F Cells were transfected with AREG siRNA (50 nM) for 24 h, and then incubated with TGF-β (10 ng/ml) for 0 ~ 24 h. The wound area (yellow square area) was quantified by image J. Data are presented as the mean ± SEM, n = 3. *p < 0.05, relative to the TGF-β-stimulated with the control siRNA group