Fig. 5
From: ABCG1 deficiency promotes endothelial apoptosis by endoplasmic reticulum stress-dependent pathway
Cholesterol repletion and depletion were correlated with endothelial apoptosis and activation of ER stress. a Cyclodextrin (CD)-cholesterol loading of control cells increased FC and CE content. CD-cholesterol loading of ABCG1-deficient EC statistically increased CE content but not FC content. Cholesterol depletion with CD lowed FC and CE content in both endothelial control and ABCG1-deficient EC. b Cholesterol repletion induced endothelial apoptosis in endothelial controls. Cholesterol depletion significantly reversed endothelial apoptosis in ABCG1-deficient EC. Apoptosis was suppressed in ABCG1-deficient EC treated with U18666A, a cholesterol transport to ER inhibitor. c, d Cholesterol repletion increased the expression of GRP78 and CHOP, and cholesterol depletion reduced the expression of GRP78 and CHOP in ABCG1-deficient EC and control cells. e, f Addition of U18666A to ABCG1-deficient EC suppressed expression of GRP78 and CHOP. Data are mean ± SD (n = 3). *P = 0.05, **P < 0.001 vs. EC controls, # P < 0.001 vs. ABCG1-deficient EC. Representative images are shown for three independent experiments