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. 2020 Apr 22;117(18):9896–9905. doi: 10.1073/pnas.1919702117

Fig. 6.

Fig. 6.

Thbs1 regulates YAP expression during neointima formation upon carotid artery ligation. (A) Diagram of LCA ligation. (B) Immunostaining of cross sections of ligated arteries with YAP (red) and Thbs1 (white) at 1 wk (n = 5), 2 wk (n = 5), and 3 wk (n = 4) after ligation in WT mice. DAPI (blue) and autofluorescence of elastin (green) are also shown. Quantification of colocalization with YAP and DAPI using Imaris colocalization software is indicated in yellow (number of nuclear YAP/total number of nuclei). (Scale bars, 50 μm.) (C) Quantification of colocalization between YAP and DAPI in B and E using Imaris colocalization software. Bars are mean ± SEM. **P < 0.01, ***P < 0.001, one-way ANOVA. (D) PLA showing cluster of Thbs1/integrin β1 (red dots, yellow arrowheads) at 3 wk after ligation in RCA and LCA. DAPI (blue) and autofluorescence of elastin (green) are also shown. (Scale bars, 50 μm.) n = 3. (E) Cross sections of ligated arteries at 3 wk postinjury in WT (n = 4), siThbs1-treated WT mice (n = 4), and Thbs1KO (n = 5) mice. Immunostaining with YAP (red), Thbs1 (white). DAPI (blue), and autofluorescence of elastin (green). Note neointima formation in WT arteries. Yellow arrowheads show nuclear localization of YAP. (Scale bars, 50 μm.)