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. Author manuscript; available in PMC: 2020 Nov 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2019 Sep 19;39(11):2261–2272. doi: 10.1161/ATVBAHA.119.313056

Figure 4. PLPP3 expression is dynamically regulated during SMC phenotypic modulation.

Figure 4.

A) Expression of the indicated genes in primary human coronary artery SMC treated with vehicle control or methyl-β-cyclodextrin (MβCD) complexed cholesterol (20μg/mL) for 48 hours to induce modulation towards a foam-cell like phenotype. Relative gene expression (fold change; mean ± SEM) was determined. B) Cell migration to vehicle (DMEM with 0.01% FBS), FBS (DMEM with 10% FBS) or LPA (DMEM with 10μM 18:1 LPA) for 24 hours (right panel; mean numbers of migrated cells ± SEM). Two-way ANOVA was used to determine differences between treatment groups and chemotaxis agent. Relative gene expression (fold change; mean ± SEM) of C) Plpp3, D) Cd68 and E) Lpar4 in primary SMCs from fl/fl and SM22-Δ on the Ldlr−/− background treated with vehicle or MβCD-cholesterol (20μg/mL) for 48 hours. Two-way ANOVA was used to determine differences between treatment groups and genotypes. F) H3K4me2 marker of the MYH11 promoter (red) visualized by ISH-PLA in aortic root sections stained with ACTA (green) and DAPI (blue). Cells positive for the H3K4me2 marker as a percentage of total CD68+ cells (cells/field quantified) in aortic root sections from fl/fl and SM22Δ animals on the Ldlr−/− background fed Western diet for 12 weeks (n=2–4/group).