Fig. 6
From: Tuftelin1 drives experimental pulmonary fibrosis progression by facilitating stress fiber assembly
TUFT1 mediated lung fibrosis in a pY256N-WASP-dependent manner. a Western blotting assay of pY256N-WASP, N-WASP, and collagen I in the lung homogenate; β-actin used as the loading control. b The relative expression of pY256N-WASP/N-WASP. c The expression of F-actin in the si-TUFT1 group, wiskostatin group, and control detected by Phalloidin staining in A549 cells, scale bars: 200 µm. d The percentage of cells with actin cores in A549 according to (c). e, f Over-expressed TUFT1 in MRC-5 cells could accelerate the matrigel contraction, and Wiskostatin could delay this phenomenon. g Over-expressed TUFT1 induced expression of pY256N-WASP and fibrosis marker FN, collagen I, and α-SMA, while wiskostatin could reverse this phenomenon detected by western-blot. h–k Corresponding optical densitometry analysis of (g) (mean ± SD). *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001