Hepcidin, an antimicrobial peptide is downregulated in ceruloplasmin-deficient mice

Peptides. 2009 Feb;30(2):262-6. doi: 10.1016/j.peptides.2008.09.017. Epub 2008 Oct 2.

Abstract

Hepcidin, a principle regulator of iron metabolism, is synthesized by the liver. Contradictory results have been reported on the regulation of hepcidin expression in response to serum transferrin saturation and liver iron content. In the present study, we explore the expression of murine hepcidin mRNA and further analyze the relationship between liver hepcidin mRNA expression, liver iron stores, and serum iron level utilizing ceruloplasmin gene knockout mice. We find that hepcidin expression correlates significantly with serum transferrin saturation, whereas there is a negative correlation of hepcidin expression with liver tissue iron level.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Infective Agents / metabolism*
  • Antimicrobial Cationic Peptides / genetics*
  • Antimicrobial Cationic Peptides / metabolism
  • Ceruloplasmin / genetics*
  • Ceruloplasmin / metabolism
  • Down-Regulation / genetics*
  • Genotype
  • Hepcidins
  • Iron / blood
  • Liver / drug effects
  • Liver / metabolism
  • Mice
  • Mice, Inbred BALB C
  • Phenotype
  • RNA, Messenger / metabolism
  • Transferrin / metabolism

Substances

  • Anti-Infective Agents
  • Antimicrobial Cationic Peptides
  • Hamp protein, mouse
  • Hepcidins
  • RNA, Messenger
  • Transferrin
  • Iron
  • Ceruloplasmin