Affordable Access

deepdyve-link
Publisher Website

Increase of E3 ubiquitin-ligase NEDD4 expression leads to degradation of its target proteins PTEN/IGF1R during the formation of goose fatty liver.

Authors
  • Chunchi, Yan1
  • Zhao, Minmeng1
  • Li, Shuo1
  • Liu, Tongjun1
  • Xu, Cheng1
  • Liu, Long1
  • Geng, Tuoyu1
  • Gong, Daoqing1
  • 1 College of Animal Science and Technology, Yangzhou University, Yangzhou, P.R. China. , (China)
Type
Published Article
Journal
Journal of animal science
Publication Date
Aug 25, 2020
Identifiers
DOI: 10.1093/jas/skaa270
PMID: 32841331
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Goose fatty liver may have a unique protective mechanism as it does not show a pathological injury even in the case of severe steatosis. Although NEDD4 participates in repair and regeneration of injured liver through its target proteins, its role in nonalcoholic fatty liver disease (NAFLD) remains unknown. Using qPCR and immunoblot analyses, here we found that the mRNA and protein expressions of NEDD4 were induced in goose fatty liver, compared to normal liver. The mRNA expression of PTEN and IGF1R was also induced in goose fatty liver, however, their protein expression was or tended to be suppressed. Moreover, co-immunoprecipitation analysis indicated that there was a physical association between NEDD4 and PTEN in goose liver, which was consistent with the ubiquitination of PTEN in goose fatty liver. Furthermore, NEDD4 overexpression in goose primary hepatocytes suppressed the PTEN and IGF1R protein level without significant effect on their mRNA expression. In conclusion, the increased expression of NEDD4 leads to the degradation of PTEN and IGF1R proteins through ubiquitination in goose fatty liver, suggesting that NEDD4 may protect goose fatty liver from severe steatosis associated injury via its target proteins during the development of goose fatty liver. © The Author(s) 2020. Published by Oxford University Press on behalf of the American Society of Animal Science. All rights reserved. For permissions, please e-mail: [email protected]

Report this publication

Statistics

Seen <100 times