Extended Data Fig. 8: SR-B1 governs LDL transcytosis in endothelial cells independent of effects on caveolae function. | Nature

Extended Data Fig. 8: SR-B1 governs LDL transcytosis in endothelial cells independent of effects on caveolae function.

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

Extended Data Fig. 8

a, Uptake of DiI–nLDL and DiI–oxLDL in endothelial cells after RNAi knockdown of SR-B1 or Pdzk1. Left, red, DiI–oxLDL; blue, DAPI-stained nuclei. n = 6 per group. b, c, Uptake (b) and transcytosis (c) of DiI–nLDL and DiI–oxLDL in cells treated with control IgG, SR-B1 blocking antibody or BLT1. n = 6 per group. d, Transcytosis of DiI–nLDL and DiI–oxLDL in endothelial cells after RNAi knockdown of SR-B1. n = 3 per group. e, f, Activation of NOS activation by VEGF (100 ng ml–1) or HDL (20 μg ml–1) with or without RNAi knockdown of SR-B1 (e, n = 10 per group) or disruption of caveolae by methyl-β-cyclodextrin (CD) treatment (f, 10 mM for 60 min, n = 8 per group). g, Abundance of target protein following RNAi knockdown of SR-B1, Pdzk1, Ldlr or Cd36 in HAECs. Findings for three samples per condition are shown. In all studies, expression of SR-B1, LDLR and CD36 was evaluated. h, i, Uptake of DiI–nLDL and DiI–oxLDL in cells depleted of LDLR by RNAi (h, n = 12 for nLDL and 13 for oxLDL) or treated with control versus LDLR blocking antibody (i, n = 6 per group). j, Transcytosis of DiI–nLDL and DiI–oxLDL in cells treated with control versus LDLR blocking antibody. n = 6 for nLDL and 3 for oxLDL. k, l, Uptake of DiI–nLDL and DiI–oxLDL in cells depleted of CD36 by RNAi (k, n = 6 per group) or treated with control versus CD36 blocking antibody (l, n = 9 and 12 for nLDL, respectively, and n = 6 for oxLDL). m, Transcytosis of DiI–nLDL and DiI–oxLDL in cells treated with control versus CD36 blocking antibody. n = 6 per group. Data are mean ± s.e.m.; P values calculated by ANOVA with Dunnett’s post-hoc test (ac) and two-sided Student’s t-test (df, h, i, k, l).

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