Exploring the role of hepcidin, an antimicrobial and iron regulatory peptide, in increased iron absorption in beta-thalassemia

Ann N Y Acad Sci. 2005;1054:417-22. doi: 10.1196/annals.1345.069.

Abstract

To develop new treatments for beta-thalassemia, it is essential to identify the genes involved in the relevant pathophysiological processes. Iron metabolism in thalassemia mice being investigated, focusing on the expression of a gene called hepcidin (Hamp), which is expressed in the liver and whose product (Hamp) is secreted into the bloodstream. In mice, iron overload leads to overexpression of Hamp, while Hamp-knockout mice suffer from hemochromatosis. The aim of this study is to investigate Hamp in the mouse model of beta-thalassemia and to address the potential gene transfer of Hamp to prevent abnormal iron absorption.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antimicrobial Cationic Peptides / biosynthesis
  • Antimicrobial Cationic Peptides / genetics
  • Antimicrobial Cationic Peptides / physiology*
  • Carcinoma, Hepatocellular / pathology
  • Cell Line / metabolism
  • Cell Line, Tumor
  • Disease Models, Animal
  • Fibroblasts / metabolism
  • Gene Expression Regulation
  • Genetic Vectors / therapeutic use
  • Hemochromatosis / genetics*
  • Hemochromatosis / metabolism
  • Hepatocytes / metabolism
  • Hepcidins
  • Humans
  • Intestinal Absorption / physiology*
  • Iron / pharmacokinetics*
  • Iron Overload / etiology*
  • Iron Overload / genetics
  • Iron Overload / metabolism
  • Lentivirus / genetics
  • Liver / metabolism
  • Liver Neoplasms / pathology
  • Mice
  • Mice, Knockout
  • NIH 3T3 Cells
  • Transduction, Genetic
  • beta-Thalassemia / metabolism
  • beta-Thalassemia / therapy

Substances

  • Antimicrobial Cationic Peptides
  • HAMP protein, human
  • Hamp protein, mouse
  • Hepcidins
  • Iron