Extended Data Fig. 3: Mutant ASXL1-derived haematopoiesis promotes atherosclerosis in Ldlr−/− mice.
a: Representative images of the whole aorta stained with Sudan IV from female Ldlr−/− mice with Vav-cre ASXL1-MT KI or control bone marrow after 12 weeks of HFHCD feeding. b: Quantification of the lesion area in the whole aorta (n = 5 female mice per group). c, d: Quantification of the lesion area in the aortic root (A) and whole aorta (B) in male Ldlr−/− mice with WT or Vav-cre ASXL1-MT KI bone marrow after 14 weeks of HFHCD feeding. (n = 5 WT, 6 Vav-cre ASXL1-MT.) e, f: Body weight and major organ weight of female (e) and male (f) Ldlr−/− mice transplanted with WT or Vav-cre ASXL1-MT KI bone marrow at the time of the atherosclerotic lesion analysis. (n = 5 WT female, 6 ASXL1-MT female, 5 WT male, 6 ASXL1-MT male.) g: The frequencies of neutrophils, total monocytes, inflammatory monocytes, and patrolling monocytes in peripheral blood cells in Ldlr−/− female mice fed the HFHCD for 12 weeks (n = 9 for each group). Data are shown as the mean ± s.d.; Unpaired two-tailed t-tests with Welch’s correction (b–g).
