Extended Data Fig. 5. Analysis of BCA lesions from gain of function mutant (m) PCSK9-AAV8 and Ldlr^−/− models of murine atherosclerosis.

(A) Schematic of experimental design for experiments using Myh11-CreER^T2/ROSA-STOP^FL/FL-eYFP mice infected once with mPCSK9-AAV8 (Myh11-CreER^T2 mPCSK9). Representative images depicting (B) EndoMT (eYFP⁻ ACTA2⁺ CD31⁺ /ACTA2⁺) and (C) MMT (eYFP⁻ ACTA2⁺ LGALS3⁺ /ACTA2⁺). (D) Quantification of Myh11-eYFP⁺ cells in the 30μm fibrous cap area. (E) Quantification of the percentage of ACTA2⁺ cells derived from SMC (Myh11-eYFP⁺ ACTA2⁺) and from non-SMC sources (Myh11-eYFP⁻ACTA2⁺) in Myh11-CreER^T2 mPCSK9 mice. (F) Quantification of MMT and EndoMT from (B & C). (G) Schematic of Ldlr^−/− Myh11-CreER^T2/ROSA-STOP^FL/FL-eYFP (Myh11-CreER^T2 Ldlr^−/−) experimental design. Representative images depicting (H) EndoMT (Myh11-eYFP⁻ ACTA2⁺ CD31⁺ /ACTA2⁺) and (I) MMT (Myh11-eYFP⁻ ACTA2⁺ LGALS3⁺ /ACTA2⁺). (J) Quantification of Myh11-eYFP⁺ cells in the 30μm fibrous cap area. (K) Quantification of the percentage of ACTA2⁺ cells derived from SMC (Myh11-eYFP⁺ ACTA2⁺) and from non-SMC sources (Myh11-eYFP⁻ ACTA2⁺) in Myh11-CreER^T2 Ldlr^−/− mice. (L) Quantification of MMT and EndoMT from (H) & (I). Scale bar: 100μm (B, C, H, I top) or 20μm (B, C, H, I bottom). Biologically independent animals are indicated as individual dots in (D, F, J, L), (E) n = 7, 6 (WT and KO: 330, 480μm), (K) n=5 (WT and KO), error bars represent mean ± SEM.