Abstract

OTU deubiquitinase 7A (OTUD7A) can suppress inflammation signaling pathways, but it is unclear whether the gene can inhibit inflammation in goose fatty liver. In order to investigate the functions of OTUD7A and identify the genes and pathways subjected to the regulation of OTUD7A in the formation of goose fatty liver, we conducted transcriptomic analysis of cells, which revealed several genes related to inflammation and immunity that were significantly differentially expressed after OTUD7A overexpression. Moreover, the expression of interferon-induced protein with tetratricopeptide repeats 5 (IFIT5), tumor necrosis factor ligand superfamily member 8 (TNFSF8), sterile alpha motif domain-containing protein 9 (SAMD9), radical S-adenosyl methionine domain-containing protein 2 (RSAD2), interferon-induced GTP-binding protein Mx1 (MX1), and interferon-induced guanylate binding protein 1-like (GBP1) was inhibited by OTUD7A overexpression but induced by OTUD7A knockdown with small interfering RNA in goose hepatocytes. Furthermore, the mRNA expression of IFIT5, TNFSF8, SAMD9, RSAD2, MX1, and GBP1 was downregulated, whereas OTUD7A expression was upregulated in goose fatty liver after 12 days of overfeeding. In contrast, the expression patterns of these genes showed nearly the opposite trend after 24 days of overfeeding. Taken together, these findings indicate that OTUD7A regulates the expression of inflammation- and immune-related genes in the development of goose fatty liver.

Highlights

  • Some fish and birds are able to pre-deposit large amounts of fat in the liver for use during migration, and the liver can return to its normal state without any obvious pathological symptoms

  • RNA sequencing analysis of the transcriptomes of goose hepatocytes transfected with the OTU deubiquitinase 7A (OTUD7A) overexpression vector vs. empty vector revealed 34 differentially expressed genes (DEGs) (19 upregulated and 15 downregulated) (Supplementary Figure S1)

  • The results from our study showed that OTUD7A regulates the expression of some immune-related genes—for example, interleukin-23 receptor (IL23R)—in goose fatty liver

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Summary

Introduction

Some fish and birds are able to pre-deposit large amounts of fat in the liver for use during migration, and the liver can return to its normal state without any obvious pathological symptoms. As the offspring of migratory birds, have this characteristic In agricultural production, this ability of geese is often used for fatty liver production. The changes that occur in goose fatty liver are physiological, with no overt injury or pathological symptoms [2,3]. Nonalcoholic fatty liver disease (NAFLD) in humans and mammals is frequently accompanied by inflammation [5,6]. The differences between geese and other animals suggest that the goose liver utilizes a protection mechanism, the underlying mechanisms remain unclear. Studies of this mechanism may provide information for developing approaches for preventing or treating NAFLD-associated complications in humans and economically important animals

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