Fig. 4
From: Tuftelin1 drives experimental pulmonary fibrosis progression by facilitating stress fiber assembly
N-WASP played an important role in the progress of TUFT1 interfering with fibrosis. a–c Knockdown of TUFT1 can inhibited the phosphorylation level of N-WASP in A549 cells. d Immunohistochemical staining of N-WASP in IPF lung tissue compare to the donor. e Immunohistochemical staining of pY256N-WASP in IPF lung tissue compare to the donor. f Immunohistochemical stain images of N-Wasp in bleomycin induced fibrosis lung tissue compare to the control. g Immunohistochemical stain images of pY256N-Wasp in bleomycin induced fibrosis lung tissue compare to the control, scale bars: 50 µm. h, i Silence the TUFT1 in MRC-5 cells could slow down the matrigel contraction compare to the control, and the sodium orthovanadate could reverse this phenomenon. j Silence the TUFT1 could decrease the expression of pY256N-WASP and α-SMA, the sodium orthovanadate could relieve the decrease level of pY256N-WASP and α-SMA in TGF-β1 treated MRC-5 cells. k–m Corresponding optical densitometry analysis of J (mean ± SD). *P < 0.05, **P < 0.01, and ***P < 0.001