SHP-1 ameliorates nonalcoholic steatohepatitis by inhibiting proinflammatory cytokine production

FEBS Lett. 2020 Sep;594(18):2965-2974. doi: 10.1002/1873-3468.13879. Epub 2020 Jul 17.

Abstract

Inflammation is the main contributor for the pathogenesis of nonalcoholic steatohepatitis (NASH). Src homology region 2 domain-containing phosphatase 1 (SHP-1, also known as PTPN6) is regarded as a negative regulator of inflammation, but its role in NASH remains unknown. Here, hepatocyte-specific Ptpn6 knockout mice (Ptpn6HKO ) and adenovirus vector-mediated ectopic expression of SHP-1 (AdSHP1) were used to evaluate the role of SHP-1 in a methionine- and choline-deficient diet-induced NASH model. Compared with the control littermates, Ptpn6HKO mice show exacerbated hepatic steatosis, inflammation, and fibrosis. Additionally, administration of AdSHP1 significantly ameliorates steatohepatitis and inhibits the expression of proinflammatory cytokines, including transforming growth factor-β, interleukin-6, and tumor necrosis factor-α. Our data indicate that SHP-1 could be a potential therapeutic target for NASH.

Keywords: Src homology domain 2-containing protein tyrosine phosphatase-1; inflammation; nonalcoholic steatohepatitis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cytokines / genetics
  • Cytokines / metabolism*
  • Disease Models, Animal
  • Inflammation / genetics
  • Inflammation / metabolism
  • Inflammation / pathology
  • Mice
  • Mice, Knockout
  • Non-alcoholic Fatty Liver Disease / metabolism*
  • Non-alcoholic Fatty Liver Disease / pathology
  • Protein Tyrosine Phosphatase, Non-Receptor Type 6 / genetics
  • Protein Tyrosine Phosphatase, Non-Receptor Type 6 / metabolism*

Substances

  • Cytokines
  • Protein Tyrosine Phosphatase, Non-Receptor Type 6
  • Ptpn6 protein, mouse