Involvement of IGFBP5 in the Development of Goose Fatty Liver via p38 Mitogen-Activated Protein Kinase (MAPK)

Abstract

Previous studies showed that insulin-like growth factor-binding protein 5 (IGFBP5) plays a role in non-alcoholic fatty liver disease; however, its expression and function in goose fatty liver remain unknown. To address this, we obtained a full-length mRNA sequence of the goose IGFBP5 gene using a 5′-rapid amplification of cDNA ends assay and nested polymerase chain reaction (PCR). Additionally, using the newly acquired sequence of 5’-untraslated region, we determined the missing sequence of the first intron. Bioinformatics analysis revealed three exons and three introns in the goose IGFBP5 gene. Quantitative PCR analysis indicated that the mRNA abundance of IGFBP5 was significantly lower in goose fatty liver than in the normal liver. Comparison of transcriptomes of goose primary hepatocytes transfected with IGFBP5 overexpression vector versus those transfected with empty vector identified 777 differentially expressed genes (DEGs). The enriched Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways indicated the focal adhesion, ECM-receptor interaction, regulation of the actin cytoskeleton, mitogen-activated protein kinase (MAPK) signaling, and GnRH signaling pathways. Immunoblotting revealed the induction of the p38 MAPK pathway by IGFBP5 overexpression, which is in line with the suppressed expression of IGFBP5 and p38 MAPK in goose fatty liver than in normal liver. These findings suggest that IGFBP5 is involved in the development of goose fatty liver via the p38 MAPK pathway.

Keywords

• goose
• fatty liver
• insulin-like growth factor-binding protein 5
• rapid amplification of cDNA end
• p38 MAPK