Fig 1: The expression of CTSC is related to asthma severity in patients.(A) The mRNA expression of CTSC in the induced sputum of patients with asthma and HCs. Data are presented as mean ± SEM. One-way ANOVA followed by Tukey’s post hoc test was used. (B and C) Pearson’s correlation analysis between CTSC expression and pulmonary function in patients with asthma. FEV1, forced expiratory volume in 1 second; FVC, forced vital capacity. (D) Pearson’s correlation analysis between CTSC expression and ACT score in patients with asthma. (E–H) Pearson’s correlation analysis between CTSC expression and related parameters of airway remodeling in patients with asthma. (I) Receiver operating characteristic analysis for the expression of CTSC to discriminate HCs from patients with SA. (J) Receiver operating characteristic analysis for the expression of CTSC to discriminate patients with MMA from patients with SA. *P < 0.05; ***P < 0.001.
Fig 2: The increased expression of CTSC impairs the epithelial barrier function.(A) Cell proliferation analysis of HBECs after CSTC silencing and overexpression using CCK-8 assay (n = 5). Two-way ANOVA followed by Tukey’s post hoc test was used. (B) Proliferation curves of HBECs after CSTC silencing and overexpression (n = 4). Two-way ANOVA followed by Tukey’s post hoc test was used. (C) A scratch test for evaluating damage repair capability in HBECs (n = 3). Two-way ANOVA followed by Tukey’s post hoc test was used. (D) Effects of CTSC expression on the permeability of HBECs monolayers (n = 3). One-way ANOVA followed by Tukey’s post hoc test was used. (E) Effects of CTSC expression on ROS generation (n = 4–8). One-way ANOVA followed by Bonferroni’s post hoc test was used. (F and G) Representative immunofluorescence of HBECs stained for E-cad and ZO-1 after CSTC overexpression (n = 3; scale bar: 50 μm). All data are presented as mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001.
Fig 3: Airway remodeling is markedly alleviated in the absence of CTSC.(A and D) Schematic of the (A) HDM model and (D) SA model. (B and E) Representative lung sections and semiquantitative analysis of mucus production (n = 5; scale bar: 50 μm). (C and F) Representative lung sections and semiquantitative analysis of peribronchial fibrosis (n = 5; scale bar: 50 μm). All data are presented as mean ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001 by 1-way ANOVA followed by Tukey’s post hoc test.
Fig 4: rhCTSC increases the activation of EMTU through activation of p38 pathway.(A) The secretion of CTSC in HBECs was detected by ELISA (n = 4). One-way ANOVA followed by Tukey’s post hoc test was used. (B) Proliferation curves of HLF-1 after rhCTSC stimulation (n = 4). Two-way ANOVA followed by Tukey’s post hoc test was used. (C) Expression of α-SMA and COL 1 protein was detected by Western blot (n = 3). Two-way ANOVA followed by Tukey’s post hoc test was used. (D) Expression of p38, p-p38, Erk, p-Erk, JNK, and p-JNK protein was detected by Western blot (n = 3). Unpaired t test was used. (E) HLF-1 were pretreated with p38 inhibitor SB203580 and then stimulated with rhCTSC. Expression of α-SMA and COL 1 protein was detected by Western blot (n = 3). Two-way ANOVA followed by Tukey’s post hoc test was used. All data are presented as mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001.
Fig 5: The activation of EMTU is markedly decreased in the absence of CTSC.(A–D) Representative immunohistochemistry images of lung tissue and semiquantitative analysis for (A) Ki67, (B) E-cad, (C) vimentin, and (D) α-SMA expression in a HDM-induced model (n = 5; scale bar: 50 μm). (E–H) Representative immunohistochemistry images of lung tissue and semiquantitative analysis for (E) Ki67, (F) E-cad, (G) vimentin, and (H) α-SMA expression in SA model (n = 5; scale bar: 50 μm). All data are presented as mean ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001 by 1-way ANOVA followed by Tukey’s post hoc test.
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