Transcription control and neuronal differentiation by agents that activate the LXR nuclear receptor family

Mol Cell Endocrinol. 1999 Sep 10;155(1-2):51-60. doi: 10.1016/s0303-7207(99)00115-x.

Abstract

LXR and PPAR receptors belong to the nuclear receptor superfamily of transcriptional activating factors. Using ligand-dependent transcription assays, we found that 5-tetradecyloxy-2-furancarboxylic acid (TOFA) transactivates chimeric receptors composed of the glucocorticoid receptor DNA binding domain and the ligand binding regions of PPARalpha, PPARbeta (NUC-1) and LXRbeta (NER) receptors. In the same assays, ligands for PPARs (oleic acid, WY-14643 and L-631,033) and LXRs (hydroxycholesterols) maintain their respective receptor selectivity. TOFA and hydroxycholesterols also stimulate transcription from a minimal fibrinogen promoter that is under the control of AP-1 or NF-kappaB transcription factor binding sites. In addition to their effects on transcription, these LXRbeta activators induce neuronal differentiation in rat pheochromocytoma cells. TOFA and the natural LXR agonist, 22 (R)-hydroxycholesterol, stimulate neurite outgrowth in 55 and 28% of cells, respectively. No neurite outgrowth was induced by the related 22(S)-hydroxycholesterol, which does not activate the LXR family. These results suggest that the hydroxycholesterol signaling pathway has a complex effect on transcription that mediates the activity of TOFA and hydroxycholesterol on neuronal differentiation in pheochromocytoma cells.

MeSH terms

  • Animals
  • Anticholesteremic Agents / pharmacology
  • COS Cells
  • Cell Differentiation / drug effects
  • Cell Line
  • Cholesterol / pharmacology
  • DNA-Binding Proteins
  • Furans / pharmacology*
  • Hypolipidemic Agents / pharmacology
  • Liver X Receptors
  • Nerve Growth Factors / pharmacology
  • Neurons / cytology
  • Neurons / drug effects
  • Neurons / physiology*
  • Oleic Acid / pharmacology
  • Orphan Nuclear Receptors
  • Peroxisome Proliferators / pharmacology
  • Pyrimidines / pharmacology
  • Rats
  • Receptors, Cytoplasmic and Nuclear / drug effects
  • Receptors, Cytoplasmic and Nuclear / physiology*
  • Receptors, Glucocorticoid / drug effects
  • Receptors, Glucocorticoid / physiology
  • Recombinant Fusion Proteins / drug effects
  • Recombinant Fusion Proteins / metabolism
  • Trans-Activators / metabolism
  • Transcription Factors / drug effects
  • Transcription Factors / physiology
  • Transcription, Genetic / drug effects*
  • Transcriptional Activation / drug effects
  • Transfection

Substances

  • Anticholesteremic Agents
  • DNA-Binding Proteins
  • Furans
  • Hypolipidemic Agents
  • Liver X Receptors
  • Nerve Growth Factors
  • Orphan Nuclear Receptors
  • Peroxisome Proliferators
  • Pyrimidines
  • Receptors, Cytoplasmic and Nuclear
  • Receptors, Glucocorticoid
  • Recombinant Fusion Proteins
  • Trans-Activators
  • Transcription Factors
  • Oleic Acid
  • 5-(tetradecyloxy)-2-furancarboxylic acid
  • pirinixic acid
  • Cholesterol