Regulation of steatohepatitis and PPARγ signaling by distinct AP-1 dimers

Cell Metab. 2014 Jan 7;19(1):84-95. doi: 10.1016/j.cmet.2013.11.018.

Abstract

Nonalcoholic fatty liver disease (NAFLD) affects up to 30% of the adult population in Western societies, yet the underlying molecular pathways remain poorly understood. Here, we identify the dimeric Activator Protein 1 as a regulator of NAFLD. Fos-related antigen 1 (Fra-1) and Fos-related antigen 2 (Fra-2) prevent dietary NAFLD by inhibiting prosteatotic PPARγ signaling. Moreover, established NAFLD and the associated liver damage can be efficiently reversed by hepatocyte-specific Fra-1 expression. In contrast, c-Fos promotes PPARγ expression, while c-Jun exerts opposing, dimer-dependent functions. Interestingly, JunD was found to be essential for PPARγ signaling and NAFLD development. This unique antagonistic regulation of PPARγ by distinct AP-1 dimers occurs at the transcriptional level and establishes AP-1 as a link between obesity, hepatic lipid metabolism, and NAFLD.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenoviridae / metabolism
  • Animals
  • Cell Line, Tumor
  • Fatty Liver / genetics
  • Fatty Liver / metabolism*
  • Fatty Liver / pathology
  • Gene Expression Regulation
  • Hepatocytes / metabolism
  • Hepatocytes / pathology
  • Humans
  • Lipid Metabolism / genetics
  • Liver / metabolism
  • Liver / pathology
  • Mice
  • Non-alcoholic Fatty Liver Disease
  • PPAR gamma / genetics
  • PPAR gamma / metabolism*
  • Protein Multimerization*
  • Proto-Oncogene Proteins c-fos / genetics
  • Proto-Oncogene Proteins c-fos / metabolism
  • Proto-Oncogene Proteins c-jun / metabolism
  • Signal Transduction*
  • Transcription Factor AP-1 / metabolism*

Substances

  • PPAR gamma
  • Proto-Oncogene Proteins c-fos
  • Proto-Oncogene Proteins c-jun
  • Transcription Factor AP-1
  • fos-related antigen 1
  • junD protein, mouse