Hepatic SOAT2 knockdown rapidly reduces cholesteryl ester levels in liver.

<p>After consuming a high cholesterol diet for 6 weeks, mice were either euthanized to collect baseline samples or were continued on diet and administered for 1 or 2 weeks control ASO or SOAT2 ASO. Quantitation of SOAT2 mRNA in liver (A) and proximal third of small intestine (B) were conducted by real-time PCR using individual RNA samples (n = 5 per treatment group). (C) Western blot analysis was used to detect hepatic SOAT2 protein expression in liver microsomes. To compare the relative expression of SOAT2 between treatment groups, the band intensity of SOAT2 was normalized to that of calnexin and quantification of protein levels was determined by densitometry (C). Fasting livers were collected and analyzed for the concentration of cholesteryl ester (CE) (D) and free cholesterol (FC) (E). All hepatic lipid values were normalized to the protein content of the extracted tissue, and represent the means ± SEM (4–6 mice per treatment group). Bars not sharing a common letter differ significantly (p<0.05).