MAP3K7CL Inhibits the Inflammatory Responses in Goose Fatty Liver.

Abstract

Inflammation often accompanies the development of liver diseases in humans, but appears to be repressed in geese. This study investigated the role of MAP3K7 C-terminal-like (MAP3K7CL) in goose fatty liver formation. Sixteen healthy 70-day-old male geese were randomly divided into control and overfed groups. Additionally, the transcriptome analysis after MAP3K7CL overexpression and lipopolysaccharide (LPS) treatment were performed in goose primary hepatocytes. The results showed that the MAP3K7CL mRNA expression was increased in the liver of overfed treatment compared to control group. Overexpression of MAP3K7CL in primary goose hepatocytes identified differentially expressed genes enriched in the mitogen-activated protein kinase (MAPK) signaling pathway. Specifically, DNA damage-inducible transcript 3 (DDIT3), insulin-like growth factor 1 receptor (IGF1R), neurofibromin 1 (NF1), and platelet-derived growth factor subunit B (PDGFB) were significantly downregulated upon MAP3K7CL overexpression, whereas heat shock protein family B member 1 (HSPB1) was significantly upregulated. Furthermore, transfection of goose hepatocytes with the MAP3K7CL overexpression vector lowered the expression of lipopolysaccharide-induced TNF factor (LITAF) and cysteinyl aspartate-specific proteinase-3, which are associated with inflammation and apoptosis, respectively. In accordance with these findings, DDIT3 and LITAF were downregulated in the overfed group, whereas HSPB1 was upregulated. Compared with the control, LPS treatment significantly decreased MAP3K7CL expression, while promoting that of LITAF and interleukin-6 (IL-6). Moreover, the combination of lipopolysaccharide and MAP3K7CL overexpression upregulated MAP3K7CL while downregulating LITAF and IL-6 with respect to LPS alone and empty vector control groups. Therefore, MAP3K7CL may inhibit the inflammatory response in goose fatty liver.