Interleukin-1beta up-regulates iron efflux in rat C6 glioma cells through modulation of ceruloplasmin and ferroportin-1 synthesis

Neurosci Lett. 2004 Jun 10;363(2):182-6. doi: 10.1016/j.neulet.2004.04.005.

Abstract

A number of pathologies, including neurodegeneration and inflammation, have been associated with iron dysmetabolism in the brain. Hence, systems involved in iron homeostasis at the cellular level have aroused considerable interest in recent years. The iron exporter ferroportin-1 (FP) and the multicopper oxidase ceruloplasmin (CP) are essential for iron efflux from cells. By using RT-PCR, we demonstrate that FP and CP gene expression is up-regulated by treatment with the pro-inflammatory cytokine IL-1beta in rat C6 cells, taken as a glial cellular model. Following stimulation with IL-1beta, a higher expression level of CP and FP was also confirmed by Western blotting. Moreover, IL-1beta has been found to increase iron efflux from C6 cells, suggesting that both proteins may play a crucial role in iron homeostasis in pathological brain conditions, such as inflammatory and/or neurodegenerative diseases.

MeSH terms

  • Animals
  • Brain / immunology
  • Brain / metabolism
  • Cation Transport Proteins / biosynthesis
  • Cation Transport Proteins / genetics*
  • Cell Line
  • Ceruloplasmin / biosynthesis
  • Ceruloplasmin / genetics*
  • Encephalitis / immunology
  • Encephalitis / metabolism
  • Glioma
  • Interleukin-1 / metabolism*
  • Interleukin-1 / pharmacology
  • Iron / metabolism*
  • Neurodegenerative Diseases / immunology
  • Neurodegenerative Diseases / metabolism
  • Neuroglia / drug effects
  • Neuroglia / metabolism*
  • RNA, Messenger / drug effects
  • RNA, Messenger / metabolism
  • Rats
  • Up-Regulation / drug effects
  • Up-Regulation / genetics*

Substances

  • Cation Transport Proteins
  • Interleukin-1
  • RNA, Messenger
  • metal transporting protein 1
  • Iron
  • Ceruloplasmin