Fig 2: Glipr1 protected CS-induced airway damage through PLAU/EGFR signaling. (A) Levels of Glipr1, Plau, Egfr, p-Egfr, and β-actin proteins in the lung tissues of mice were measured by Western blotting analysis. Quantitative analysis of (B) Glipr1, (C) Plau, (D) Egfr, and (E) p-Egfr. (F) mRNA levels and (G) protein expression in bronchoalveolar lavage fluid (BALF) of Plau. (H) IHC. Error bars represent SD. *P < 0.05; **P < 0.01; ***P < 0.001.

Fig 3: GLIPR1 activated the TIMP1-CD63-ITGB1-AKT signaling pathway. Protein levels of GLIPR1, TIMP1, CD63, ITGB1, and AKT in SHC-44 (A) and SW1783 (B) cells were detected by western blot. The relative expression of GLIPR1, TIMP1, CD63, ITGB1, and AKT was calculated via normalization to β-actin expression. (*) represents a significance compared with the Model group. *, P<0.05; **, P<0.01; ***, P<0.001; ****, P<0.0001. NC, normal group; Model, model group.

Fig 4: Glipr1 knockout caused more severe inflammatory infiltration after cigarette smoke exposure. (A) Total protein levels, (B) total cell counts, (C) neutrophils, (D) macrophages, and (E) lymphocytes in bronchoalveolar lavage fluid (BALF) were assessed. IL-6 concentrations in (F) BALF and (G) plasma samples were measured by ELISA. (H) MMP-9 concentration in BALF were measured by ELISA. (I) Ratio of MMP-9/TIMP-1 in the BALF. Error bars represent SD. *P < 0.05; **P < 0.01; ***P < 0.001.

Fig 5: GLIPR1 affected the proliferation of ACM cells. (A) The effect of GLIPR1 on the proliferation of SHC-44 cells at different culture times (0, 24, 36, and 48 h). (B) The effect of GLIPR1 on the proliferation of SHC-44 cells at different culture times (0, 24, 36, and 48 h). (*) and (#) represent a significance compared with the Model and NC group, respectively. *, P<0.05; **, P<0.01; ##, P<0.01. NC, normal group (SVG p12 cells); Model, model group. ACM, astrocytoma.