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The impact of defective cholesterol metabolism on sex-specific hepatocarcinogenesis in hepatocyte specific deletion of Cyp51 in mice

ABSTRACT: The impact of defective cholesterol metabolism on sex-specific hepatocarcinogenesis in hepatocyte specific deletion of Cyp51 in mice

PROVIDER: PRJNA525370 | ENA |

REPOSITORIES: ENA

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The impact of defective cholesterol metabolism on sex-specific hepatocarcinogenesis in hepatocyte specific deletion of Cyp51 in mice

Project description:The potential role of defective cholesterol metabolism in HCC development and exposition the Cyp51 gene as a promising marker with tumor suppressor potential in sex-dimorphic chronic liver pathogenesis in mice. Hepatocyte-specific Cyp51 knock-out (KO) and wild type (WT) mice on a mixed background (129/Pas (10%) × C57BL/6J (90%)) of both sexes (F and M) were investigated at the age of 24 months. From each of KO mice, two samples (a tumor and a surrounding tissue) were considered.

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Project description:Cholesterol is one of the key molecules in mammals and the most striking examples of its deficiency are the inborn errors of cholesterol biosynthesis that manifest in severe whole body phenotypes. Liver, the principal site of cholesterol homeostasis, has rarely been investigated in these defects. We thus focused on the hepatocyte-specific deletion of lanosterol 14α-demethylase (CYP51) catalyzing the rate-limiting step in the post-squalene part of cholesterol synthesis. Liver-specific Cyp51 KO (LKO or K) and littermate control (LWT or W) mice (129/Pas (10%) × C57BL/6J (90%)) of both sexes (F and M) were investigated in the context of different nutritional availability of fat and cholesterol (standard laboratory diet without cholesterol (LFnC or L), high-fat diet without cholesterol (HFnC or H) and high-fat diet with cholesterol (HFC or C) due to the known sexual dimorphism in hepatic gene expression, where lipid metabolic pathways are among the most biased. 3 condition experimental design: 3 diets (LFnC or L, HFnC or H, HFC or C), 2 genotypes (LWT or W, LKO or K), 2 sexes (F, M), 3 biological replicates per condition, 36 mice altogether

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