Potential interplay between NFκB and PPARγ in human dermal microvascular endothelial cells cultured in low magnesium

Magnes Res. 2014 Apr-Jun;27(2):86-93. doi: 10.1684/mrh.2014.0365.

Abstract

Dermal microvascular endothelial cells contribute to cutaneous inflammation by secreting proinflammatory cytokines and chemokines. We show here that low extracellular magnesium stimulates the secretion of interleukin 8 and monocyte chemoattractant protein-1 in dermal microvascular endothelial cells. This secretory pattern might result from interplay between NFκB, the master regulator of inflammation, and PPARγ, a transcription factor that has emerged as an inhibitor of inflammation. Indeed, both NFκB and PPARγ are activated in dermal microvascular endothelial cells cultured in low magnesium-containing medium. In conclusion, we hypothesize that PPARγ and NFκB might contribute to the response of these cells to low Mg.

Keywords: NFκB; PPARγ; chemokines; magnesium; microvascular endothelial cells.

MeSH terms

  • Cells, Cultured
  • Dermis / cytology
  • Dermis / drug effects
  • Dermis / metabolism*
  • Endothelial Cells / drug effects
  • Endothelial Cells / metabolism*
  • Humans
  • Magnesium / administration & dosage*
  • Microcirculation / drug effects
  • Microcirculation / physiology*
  • NF-kappa B / metabolism*
  • PPAR gamma / metabolism*

Substances

  • NF-kappa B
  • PPAR gamma
  • Magnesium