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 30 μm 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: 100 μm (b,c,h,i top) or 20 μm (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, 480 μm), (k) n=5 (WT and KO), error bars represent mean ± SEM.