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Possible association of arrestin domain-containing protein 3 and progression of non-alcoholic fatty liver disease.

Authors
  • Ogawa, Masahiro1
  • Kanda, Tatsuo1
  • Higuchi, Teruhisa1
  • Takahashi, Hiroshi1
  • Kaneko, Tomohiro1
  • Matsumoto, Naoki1
  • Nirei, Kazushige1
  • Yamagami, Hiroaki1
  • Matsuoka, Shunichi1
  • Kuroda, Kazumichi1
  • Moriyama, Mitsuhiko1
  • 1 Division of Gastroenterology and Hepatology, Department of Medicine, Nihon University School of Medicine, 30-1 Oyaguchi-kamicho, Itabashi-ku, Tokyo 173-8610, Japan. , (Japan)
Type
Published Article
Journal
International Journal of Medical Sciences
Publisher
Ivyspring International Publisher
Publication Date
Jan 01, 2019
Volume
16
Issue
7
Pages
909–921
Identifiers
DOI: 10.7150/ijms.34245
PMID: 31341404
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

The prevalence of non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) is increasing worldwide. Several effective drugs for these diseases are now in development and under clinical trials. It is important to reveal the mechanism of the development of NAFLD and NASH. We investigated the role of arrestin domain-containing protein 3 (ARRDC3), which is linked to obesity in men and regulates body mass, adiposity and energy expenditure, in the progression of NAFLD and NASH. We performed knockdown of endogenous ARRDC3 in human hepatocytes and examined the inflammasome-associated gene expression by real-time PCR-based array. We also examined the effect of conditioned medium from endogenous ARRDC3-knockdown-hepatocytes on the apoptosis of hepatic stellate cells. We observed that free acids enhanced the expression of ARRDC3 in hepatocytes. Knockdown of ARRDC3 could lead to the inhibition of inflammasome-associated gene expression in hepatocytes. We also observed that conditioned medium from endogenous ARRDC3-knockdown-hepatocytes enhances the apoptosis of hepatic stellate cells. ARRDC3 has a role in the progression of NAFLD and NASH and is one of the targets for the development of the effective treatment of NAFLD and NASH.

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