Extended Data Fig. 2: Conserved and divergent responses to sustained atherogenic dyslipidemia.
From: Kupffer cells dictate hepatic responses to the atherogenic dyslipidemic insult
a, Plasma levels of cholesterol in dyslipidemic APOE cKO and D374Y mice with respective littermate controls, maintained on a high fat diet for 20 weeks. (APOE cKO n = 16 vs 11; and D374Y n = 7 vs 3). Plots are ± SEM, two-sided t-test b, Representative liver sections stained with ORO in APOE cKO and D374Y mice after 20 weeks on a high fat diet (scale bars = 100 μm, n = 2 vs 2 for D374Y and n = 3 vs 3 for APOE cKO, where n indicates a different mouse). c, Representative liver sections stained with H&E in APOE cKO and D374Y mice after 20 weeks on a high fat diet (scale bars = 100 μm, n = 2 vs 2 in each group where n indicates a different mouse).d, Unique and common upregulated genes in both strains at 8, 12, and 20 weeks on a high fat diet. Unique genes for each strain are indicated at the bottom. e, Flow cytometry of CLEC4F levels on Kupffer cells from female D374Y versus littermate control after 8 weeks of high fat diet. f, Heatmap of the 72 genes upregulated at all time points in both strains, expressed in 76 human single cell types. g, Flow cytometry plots showing percentages of blood and liver monocytes, and liver Kupffer cells in dyslipidemic D374Y mice given clodronate liposome or Dil liposomes control for 8 weeks while on a high fat diet. h, Immunohistochemistry of liver to detect CD5L production in control or clodronate treated D374Y mice after 8 weeks of high fat diet (scale bars = 100 μm). i, The 14 genes not affected by clodronate-induced Kupffer cells depletion, expressed in liver myeloid cell clusters. j, Correlation between plasma IL18BP and liver PCSK9 expression in humans.
