Fig. 3: Hypercholesterolemia is the only trigger for KCs proliferation, pool expansion and foamy phenotype. | Nature Communications

Fig. 3: Hypercholesterolemia is the only trigger for KCs proliferation, pool expansion and foamy phenotype.

From: Loss of embryonically-derived Kupffer cells during hypercholesterolemia accelerates atherosclerosis development

Fig. 3

A Experimental plan for ezetimibe treatment to block intestinal cholesterol absorption. B Feeding ezetimibe to Ldlr−/− male mice fed HC diet blocked plasma cholesterol elevation (chow vs HC and HC vs HC + Eze: ****p < 0.0001), resulting in (C) no increased proliferation (as determined by KI-67 staining; chow vs HC: ***p = 0.0002 and HC vs HC + Eze: **p = 0.004) (D), no increased pool density (chow vs HC: ***p = 0.0008 and HC vs HC + Eze: **p = 0.002), and (E) no lipid loading (bodipy; chow vs HC and HC vs HC + Eze: ****p < 0.0001) of KCs. (n = 4, 4 and 3 for chow-, HC- and HC + eze-fed mice, respectively). All data in this figure are from one experiment and presented as mean values ± SEM. Statistical significance tested with 1-way ANOVA and Tukey multiple comparison test. Source data are provided as a Source Data File.

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