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. Author manuscript; available in PMC: 2022 Oct 11.
Published in final edited form as: Dev Cell. 2021 Sep 27;56(19):2765–2782.e10. doi: 10.1016/j.devcel.2021.09.001

Figure 7: H3K4me2 editing inhibits SMC investment in the neointima after vascular injury.

Figure 7:

A. Mason staining of ligated carotid cross sections. Scale bar = 100 μm. B. Morphometric analysis of neointima and media area in Myocd-LSD1 and Myocd-LSD1NF infected carotids. N = 9-12 mice per group. C. Immunofluorescent staining for YFP, ACTA2, MYH11, and DAPI on cross-sections from ligated right carotids infected with Myocd-LSD1 or Myocd-LSD1NF. Scale bar = 100 μm. D. Percentage of neointimal lesion populated by YFP+ SMC. N = 9-12 mice per group. E. Scratch wound assay on Myocd-LSD1NF and Myocd-LSD1 SMC. Representative images at baseline or after 24h treatment with PDGF-BB (30 ng/ml). Scale bars: 100 μm. F. Quantification of SMC migration: percentage closure normalized to the wound area at baseline. G. Immunofluorescent staining of cytoskeleton components: F-actin (phalloidin), ACTA2, and Talin in Myocd-LSD1NF and Myocd-LSD1 SMC. Scale bar: 50 μm. Data are represented as mean ± s.e.m of 9-12 independent biological replicates. Groups were compared by unpaired Student t-test, Fisher’s exact test, or Two-Way ANOVA. * p<0.05, ** p<0.001, *** p<0.0001.