Extended Data Fig. 5: Endothelial SR-B1 does not influence vascular inflammation. | Nature

Extended Data Fig. 5: Endothelial SR-B1 does not influence vascular inflammation.

From: SR-B1 drives endothelial cell LDL transcytosis via DOCK4 to promote atherosclerosis

Extended Data Fig. 5

a, qRT–PCR was used to compare Cd68 transcript levels in aortas from Apoe−/−SR-B1fl/fl and Apoe−/−SR-B1∆EC male mice, n = 8 per group. bi, mRNA abundance was also evaluated for the following genes, using Hprt1 as a housekeeping gene and normalizing expression to Cd68 levels: E-selectin (Sele; b), P-selectin (Selp; c), Vcam1 (d), Icam1 (e), Tgfb1 (f), Tnf (g), Il6 (h), and Il10 (i), with n = 8 per group. j, Representative still images of leukocyte–endothelial cell adhesion evaluated by intravital microscopy in the mesenteric microcirculation of Apoe−/−SR-B1fl/fl and Apoe−/−SR-B1∆EC male mice administered vehicle (n = 10 and 11, respectively) or TNF (n = 5 and 6, respectively). k, Summary data for leukocyte velocity in four study groups in j. l, Gating strategy for evaluation of CD45+F4/80+ cell number and uptake of DiI–LDL in the aorta. Following digestion of the aorta, all cells were first gated in FSC/SSC according to cell size and granularity. The resulting population was gated according to cell viability using DAPI. DAPI-negative live cells were gated for positivity for CD45, and CD45+ cells were then gated for positivity for F4/80 and the DiI label. Data are mean ± s.e.m.; in k, P values calculated by ANOVA with Dunnett’s post-hoc test.

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