High-level expression of RXRα and the presence of endogenous ligands contribute to expression of a peroxisome proliferator-activated receptor- responsive gene in hepatoma cells

Andrea Galli, Mark Stewart, Ryan Dorris, David Crabb

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24 Scopus citations


Genes containing peroxisome proliferator-activated receptor (PPAR) binding sites are both inducible by peroxisome proliferators and expressed in a tissue-specific fashion. A PPAR-responsive reporter gene cotransfected with a PPARα expression vector was highly expressed in H4IIEC3 hepatoma cells. Addition of clofibrate resulted in a modest further induction of the reporter gene. In CV-1 cells, high expression of the reporter required the addition of clofibrate. H4IIEC3 cells had higher levels of retinoid X receptor (RXRα) than CV-1 cells; cotransfection of CV-1 cells with PPARα plus RXRα expression plasmids abolished the cell line difference in basal and clofibrate-stimulated expression of the reporter. Lipid extracts of hepatoma cells or of liver or kidney stimulated expression of the reporter; extracts of CV-1 cells were far less effective. Chromatographic analysis of these extracts revealed high levels of three fractions of lipid in liver and H4IIEC3 cells that were lower in CV-1 cells. We conclude that (1) in cells expressing high levels of both RXRs and PPARα, such as hepatocytes and kidney cells, these factors are constitutively active; (2) activators of PPARα may increase its ability to form heterodimers with RXRs when the latter are limiting; and (3) hepatoma cells, liver, and kidney contain lipid- extractable compounds capable of activating PPARα.

Original languageEnglish (US)
Pages (from-to)288-294
Number of pages7
JournalArchives of Biochemistry and Biophysics
Issue number2
StatePublished - Jun 15 1998



  • Clofibrate
  • Lipid
  • Liver
  • Retinoid
  • Tissue specificity

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

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