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. Author manuscript; available in PMC: 2021 May 3.
Published in final edited form as: Circ Res. 2021 Feb 24;128(9):1258–1275. doi: 10.1161/CIRCRESAHA.120.318688

Figure 3. The knockdown of CARMN regulated hCASMC proliferation, migration and dedifferentiation.

Figure 3

A) Representative FACS plots showing the of EdU uptake in hCASMCs transfected with GapmeR targeting CARMN (GapCARMN) or GapmeR control (GapCTR). The gate (P4) indicates the EdU positive cells, the samples are named GapmeR negative control (GapCTR) and GapmeR targeting CARMN (GapCARMN). B) Percentage of EdU positive hCASMCs (n=3) following transfection with GapCARMN, GapCTR and un-transfected cells (Mock) upon PDGF-BB stimuli and in 0.2% FBS. Oneway ANOVA with Bonferroni multiple comparison test was used to assess statistical significance indicated with p values. C) Representative pictures of hCASMCs at 0 and 10 hours from the scratch following transfection with GapCARMN, GapCTR and Mock in 0.2% FBS medium. Pictures were acquired at 10X magnification. Scale bar 100μm. D) Quantification of the relative migration distances of hCASMCs (n=3), obtained using ImageJ tool. One-way ANOVA with Bonferroni multiple comparison test was used to assess statistical significance indicated with p values. E), F), G), H) Expression levels of dedifferentiation markers Acta2, Myh11, CD68 and Lgals3 in hCASMCs (n=3) stimulated with water-soluble cholesterol-methyl-b-cyclodextrin (CMBCD) or 0.2% BSA for 72 hours following transfection with GapCARMN, GapCTR or Mock. One-way ANOVA with Bonferroni multiple comparison test was used to assess statistical significance indicated with p values.