Fig. 7.

KLK8 exerts biological effects through the activation of the PAR1 receptor, which is involved in HG-PA-induced differentiation, collagen synthesis, and the migration of CFs.  A–D OE-KLK8-treated CFs were continuously transfected for 12 h. Interventions were performed using the PAR1 and PAR2 antagonists SCH79797 and FSLLRY-NH2. E-G. The PAR1 antagonist SCH79797 was used to treat HG-PA-exposed CFs. A OE-KLK8-overexpressing CFs were treated with the PAR1 antagonist SCH79797 (10 µM) or the PAR2 antagonist FSLLRY-NH2 (1 µM). The MTT assay was performed to determine the proliferation rate of the cells; *P  < 0.05 vs. control; # P  < 0.05 vs. OE-KLK8. B Immunoblotting of KLK8 and the fibrosis-associated proteins α-SMA, TGFβ1, Collagen I, and Collagen III. C Immunofluorescence staining of α-SMA (green); the nuclei were restained with DAPI (blue); scale bar = 50 μm. D Wound healing assay; scale bar = 50 μm. E Immunoblotting of KLK8 and the fibrosis-associated proteins α-SMA, TGFβ1, Collagen I, and Collagen III. F Immunofluorescence staining of α-SMA (green). The cell nuclei were restained with DAPI (blue); scale bar = 50 μm. G Wound healing assay; scale bar = 50 μm. The data are expressed as the mean ± SEM of three independent experiments; *p  < 0.05, **p  < 0.01, ***p  < 0.001, and ****p  < 0.0001.