Fig 2: Reduction of PD-L1 levels in Β16F10 cells by selectively targeting the RGDKGE collagen fragment depends on YAP. (A) Western blot analysis of nuclear extracts for YAP or loading control TBP in Β16F10 cells treated with anti-RGDKGE collagen fragment antibody (Mab XL313) or non-specific control (Ab Cont). (B) Western blot analysis of cell whole cell lysates for YAP or loading control tubulin in control non-targeting shRNA (NT-shRNA) and Yap-shRNA knock down Β16F10 cells. (C) Western blot analysis of whole cell lysates for PD-L1 or loading control tubulin in non-attached control transfected Β16F10 cells (Β16F10-NT) treated with anti-RGDKGE collagen fragment antibody (Mab XL313) or non-specific control (Ab Cont). (D) Western blot analysis of whole cell lysates for PD-L1 or loading control tubulin in non-attached Yap-knock down transfected Β16F10 cells (Β16F10-YAP/K/D) treated with anti-RGDKGE collagen fragment antibody (Mab XL313) or non-specific control (Ab Cont). PD-L1, programmed death-ligand 1; shRNA, short hairpin RNA; Mab, monoclonal antibody.

Fig 3: PTX activates the Wnt/β-catenin signaling pathway. (A) The effect of baseline PTX levels on the Wnt/β-catenin signaling pathway. (B) The effect of PTX in conjunction with Wnt3a on the Wnt/β-catenin signaling pathway, Wnt3a was transfected with TOPFlash in HEK293 cells for 48 h, PTX or PBS were directly added to the transfected cells at varying concentrations, as indicated. RLU, relative light units. (C and D) Representative immunoblots and densitometry analysis showing cytoplasmic p-β-catenin, c-Myc, and nuclear β-catenin in the spinal cords of mice on postoperative day 21. β-actin and TBP was used as the loading control respectively. Data are presented as mean ± sem, *P<0.05, **P<0.01, ***P<0.001. n=3 or more in each group