Extended Data Fig. 3: Endothelial SR-B1 promotes atherosclerosis in LDLR null mice by driving LDL entry into the artery wall.
From: SR-B1 drives endothelial cell LDL transcytosis via DOCK4 to promote atherosclerosis
a, Representative in situ aortic arch images of atherosclerotic plaque (yellow arrows) in male Ldlr−/−SR-B1fl/fl and Ldlr−/−SR-B1∆EC mice. b, Representative lipid-stained en face images of aortas. c, Lesion areas in en face aortas (per cent of total surface area); n = 10 and 8 for Ldlr−/−SR-B1fl/fl and Ldlr−/−SR-B1∆EC, respectively. d, Representative lipid and haematoxylin-stained aortic root sections (lesions outlined by yellow dashed line, magnification 40×). e, Lesion areas in aortic root sections; n = 10 and 8, respectively. f–h, Plasma total cholesterol (f), triglyceride (g), and HDL cholesterol (h); n = 10 and 8, respectively. i, Representative lipoprotein profiles. j, k, DiI–nLDL uptake in the aorta. Human apolipoprotein B abundance (j) or DiI fluorescence intensity (k) was evaluated in aorta homogenates 4 h after intravenous DiI–nLDL injection. j, Left, representative immunoblot with three samples per group; j, k, n = 5 and 4 for Ldlr−/−SR-B1fl/fl and Ldlr−/−SR-B1∆EC, respectively. l, m, Uptake of DiI-labelled mouse LDL (l) or mouse VLDL/IDL (m) in aorta from Ldlr−/−SR-B1fl/fl and Ldlr−/−SR-B1∆EC mice (n = 4 and 5, respectively). Data are mean ± s.e.m., P values calculated by two-sided Student’s t-test.
