(A) Representative confocal IF images of ITGAV clusters in dermal fibroblasts incubated with or without WNT5A (n = 4 for each group). (B) Representative Western blots of P-PAXILLIN, PAXILLIN, P-TALIN and TALIN (n = 3 for each group). (C) Representative confocal images, z-stack reconstructions, and Venn diagrams showing colocalization of LAP with ITGAV and P-PAXILLIN, and 3 -dimensional scatter plots showing the distribution of each marker at each localization (n ≥ 10 for each group); schematic overview of the experimental conditions and areas of assessment. Pearson’s r is the Pearson’s correlation coefficient between LAP-ITGAV and P-PAXILLIN voxel intensities. M1 and M2 representing for Manders’ split coefficients. (D) Schematic illustration of the experiment for measuring the rupture force with magnetic tweezers. (E) Violin plots showing the force required to rupture magnetic beads coupled with peptides containing the RGD domain of LAP-TGF-β1 (RRGDLATISPASSKGGGGSRLLLLLLR) from the cell surface of dermal fibroblasts incubated with WNT5A with or without ITGAV inhibitor (ITGAVi) (n ≥ 50 for each group). (F) Levels of active TGF-β in the cell culture supernatant of dermal fibroblasts incubated with WNT5A with or without ITGAVi (n = 6 for each group). (G) Representative Western blots of P-SMAD3 in dermal fibroblasts stimulated by WNT5A with and without the ITGAVi (n = 3 for each group). The black thin vertical lines were drawn to separate noncontiguous lanes. (H) Representative Trichrome stainings and (I) Quantification of the dermal thickness, the hydroxyproline content, myofibroblast counts, and active TGF-β in the skin tissue of WNT5A-induced skin fibrosis mice treated with or without ITGAVi (n = 5 for each group). Results are shown as median ± IQR. The statistical significance was determined by 1-way ANOVA with Tukey’s multiple comparison test. Adv, Adenovirus.