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
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Antimicrobial Cationic Peptides / biosynthesis
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Antimicrobial Cationic Peptides / genetics
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Antimicrobial Cationic Peptides / physiology*
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Carcinoma, Hepatocellular / pathology
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Cell Line / metabolism
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Cell Line, Tumor
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Disease Models, Animal
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Fibroblasts / metabolism
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Gene Expression Regulation
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Genetic Vectors / therapeutic use
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Hemochromatosis / genetics*
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Hemochromatosis / metabolism
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Hepatocytes / metabolism
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Hepcidins
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Humans
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Intestinal Absorption / physiology*
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Iron / pharmacokinetics*
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Iron Overload / etiology*
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Iron Overload / genetics
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Iron Overload / metabolism
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Lentivirus / genetics
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Liver / metabolism
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Liver Neoplasms / pathology
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Mice
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Mice, Knockout
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NIH 3T3 Cells
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Transduction, Genetic
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beta-Thalassemia / metabolism
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beta-Thalassemia / therapy
Substances
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Antimicrobial Cationic Peptides
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HAMP protein, human
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Hamp protein, mouse
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Hepcidins
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Iron