Research Paper Volume 16, Issue 8 pp 7217—7248

Hepatocyte-specific METTL3 ablation by Alb-iCre mice (GPT), but not by Alb-Cre mice (JAX), resulted in acute liver failure (ALF) and postnatal lethality


Figure 3. Hepatic METTL3 homozygous knockout by Alb-iCre mice (GPT) induces abnormal lipid accumulation in mouse hepatocytes. (AC) Representative H&E staining photographs of liver sections from control mice and METTL3Δhep mice (GPT) at 4 (A), 7 (B) and 14 (C) days postnatally. Scale bar = 100 μm. (D) Heatmap depicts the differential expression of hepatic lipid metabolism-related genes from RNA-seq results deposited in NCBI GEO under the accession number GSE198512 [17]. In the cluster heatmap, class comparison and hierarchical clustering of differentially expressed genes (DEGs) involved in hepatic lipid metabolism were performed between control mice and METTL3Δhep mice (GPT) at 2 weeks after birth. Genes with increased and reduced expressions are shown in red and blue, respectively. (E) GO analysis of up- and downregulated genes related with hepatic lipid metabolism (from RNA-seq data deposited in GEO under accession number GSE198512) in the liver of control mice and METTL3Δhep mice (GPT) at 2 weeks after birth. (F) qRT-PCR analysis of the mRNA expression of genes related with to fatty acid oxidation, cholesterol efflux, lipid metabolic process, lipid transport and lipid biosynthetic process in the livers of METTL3Δhep mice (GPT).