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. 2021 Mar 8;8(10):2004000. doi: 10.1002/advs.202004000

Figure 4.

Figure 4

The influence of RAC1‐YAP signaling regulates collective spreading in vitro and wound healing in vivo. A) Immunofluorescence staining showing that activation of RAC1 enhanced YAP expression and actin organization on soft substrates. Scale bar, 100 µm. B) Treatment with RAC1 activator increased YAP nuclear‐to‐cytoplasmic ratios in the periphery and the center. C) Immunofluorescence staining showing that the activation of RAC1 enhanced RAC1 expression and actin organization on soft substrates. Scale bar, 100 µm. D,E) Quantification of spreading area and spreading trail of spheroids indicating that RAC1 activation enhanced cell movement on soft substrates. F) RT‐qPCR quantification revealing the downregulation of small GTPase transcript markers (RAC1, ROCK1, SRF, MRTFB) and YAP on the soft substrate, with significant upregulation after the activation of RAC1. G) Model of connective tissue defect on mouse skin. H) Immunofluorescence staining showing that the expression of RAC1–YAP signaling gradually decreased from the regeneration boundary to the back. Scale bars, 100 µm in wide‐fields; 50 µm in insets. The top view of immunofluorescence staining of the entire defect area I) and quantitative analysis of the mouse skin defect area J) indicate that RAC1 inhibition prohibited healing of the collective tissue defect. Scale bar, 1 mm. Data are the means ± SEM. *P < 0.05 versus corresponding soft matrix group, †P < 0.05 versus corresponding stiff matrix+RAC1 inhibitor group, one‐way ANOVA.