Anemia in beta-thalassemia patients targets hepatic hepcidin transcript levels independently of iron metabolism genes controlling hepcidin expression

Haematologica. 2008 Jan;93(1):111-5. doi: 10.3324/haematol.11656.

Abstract

Thalassemia associates anemia and iron overload, two opposite stimuli regulating hepcidin gene expression. We characterized hepatic hepcidin expression in 10 thalassemia major and 13 thalassemia intermedia patients. Hepcidin mRNA levels were decreased in the thalassemia intermedia group which presented both lower hemoglobin and higher plasma soluble transferrin receptor levels. There was no relationship between hepcidin mRNA levels and those of genes controlling iron metabolism, including HFE, hemojuvelin, transferrin receptor-2 and ferroportin. These results underline the role of erythropoietic activity on hepcidin decrease in thalassemic patients and suggest that mRNA modulations of other studied genes do not have a significant impact.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Anemia / complications*
  • Antimicrobial Cationic Peptides / biosynthesis*
  • Cation Transport Proteins / biosynthesis
  • Female
  • GPI-Linked Proteins
  • Gene Expression Regulation*
  • Hemochromatosis Protein
  • Hepcidins
  • Histocompatibility Antigens Class I / biosynthesis
  • Humans
  • Iron / metabolism*
  • Liver / metabolism*
  • Male
  • Membrane Proteins / biosynthesis
  • Middle Aged
  • Receptors, Transferrin / biosynthesis
  • beta-Thalassemia / complications*

Substances

  • Antimicrobial Cationic Peptides
  • Cation Transport Proteins
  • GPI-Linked Proteins
  • HAMP protein, human
  • HFE protein, human
  • HJV protein, human
  • Hemochromatosis Protein
  • Hepcidins
  • Histocompatibility Antigens Class I
  • Membrane Proteins
  • Receptors, Transferrin
  • TFR2 protein, human
  • metal transporting protein 1
  • Iron