PPARγ population shift produces disease-related changes in molecular networks associated with metabolic syndrome

Cell Death Dis. 2011 Aug 11;2(8):e192. doi: 10.1038/cddis.2011.74.

Abstract

Peroxisome proliferator-activated receptor gamma (PPARγ) is a key regulator of adipocyte differentiation and has an important role in metabolic syndrome. Phosphorylation of the receptor's ligand-binding domain at serine 273 has been shown to change the expression of a large number of genes implicated in obesity. The difference in gene expression seen when comparing wild-type phosphorylated with mutant non-phosphorylated PPARγ may have important consequences for the cellular molecular network, the state of which can be shifted from the healthy to a stable diseased state. We found that a group of differentially expressed genes are involved in bi-stable switches and form a core network, the state of which changes with disease progression. These findings support the idea that bi-stable switches may be a mechanism for locking the core gene network into a diseased state and for efficiently propagating perturbations to more distant regions of the network. A structural analysis of the PPARγ-RXRα dimer complex supports the hypothesis of a major structural change between the two states, and this may represent an important mechanism leading to the differential expression observed in the core network.

MeSH terms

  • Dimerization
  • Gene Expression Regulation
  • Humans
  • Metabolic Networks and Pathways*
  • Metabolic Syndrome / metabolism*
  • PPAR gamma / chemistry
  • PPAR gamma / genetics*
  • PPAR gamma / metabolism*
  • Phosphorylation
  • Protein Structure, Tertiary
  • Retinoid X Receptor alpha / metabolism

Substances

  • PPAR gamma
  • Retinoid X Receptor alpha