Downregulation of hepcidin and haemojuvelin expression in the hepatocyte cell‐line HepG2 induced by thalassaemic sera
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Summary: β‐Thalassaemia represents a group of diseases, in which ineffective erythropoiesis is accompanied by iron overload. In a mouse model of β‐thalassaemia, we observed that the liver expressed relatively low levels of hepcidin, which is a key factor in the regulation of iron absorption by the gut and of iron recycling by the reticuloendothelial system. It was hypothesised that, despite the overt iron overload, a putative plasma factor found in β‐thalassaemia might suppress liver hepcidin expression. Sera from β‐thalassaemia and haemochromatosis (C282Y mutation) patients were compared with those of healthy individuals regarding their capacity to induce changes the expression of key genes of iron metabolism in human HepG2 hepatoma cells. Sera from β‐thalassaemia major patients induced a major decrease in hepcidin (HAMP) and lipocalin2 (oncogene 24p3) (LCN2) expression, as well as a moderate decrease in haemojuvelin (HFE2) expression, compared with sera from healthy individuals. A significant correlation was found between the degree of downregulation of HAMP and HFE2 induced by β‐thalassaemia major sera (r = 0·852, P < 0·0009). Decreased HAMP expression was also found in HepG2 cells treated with sera from β‐thalassaemia intermedia patients. In contrast, the majority of sera from hereditary haemochromatosis patients induced an increase in HAMP expression, which correlated with transferrin (Tf) saturation (r = 0·765, P < 0·0099). Our results suggest that, in β‐thalassaemia, serum factors might override the potential effect of iron overload on HAMP expression, thereby providing an explanation for the failure to arrest excessive intestinal iron absorption in these patients.
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The hypoxic response (decreased hepcidin) seems to dominate that due to inflammation (increased hepcidin) even when iron levels are high.
“with in many cases the hypoxic response (decreased hepcidin) seeming to dominate that due to inflammation (increased hepcidin) even when iron levels are high [352,353].”
Thalassaemia predisposes towards PE and causes hepcidin to decrease and NGAL to increase, with consequent iron dysregulation.
“We note in this context that thalassaemia not only predisposes towards PE but is known in general to cause hepcidin to decrease and NGAL to increase [352,353,356,535], with consequent and inevitable iron dysregulation.”
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Iron Metabolism in Thalassemia and Sickle Cell Anemia: The influence of Genetic ModifiersPreprint
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Self-citation
- Authors
- Weizer‐Stern, O., Adamsky, K., Amariglio, N., Levin, C., Koren, A., Breuer, W., Rachmilewitz, E., Breda, L., Rivella, S., Ioav Cabantchik, Z., & Rechavi, G.
- Affiliations
- Tel Aviv University (IL)
- Emek Medical Center (IL)
- Hebrew University of Jerusalem (IL)
- Wolfson Medical Center (IL)
- Cornell University (US)
- Corresponding author
- Rechavi, Gideon
- Venue
- British Journal of Haematology
- Publisher
- Wiley
- Published
- 2006-08-31
- Volume
- 135
- Issue
- 1
- Pages
- 129-138
- ISSN
- 0007-1048 (ISSN-L)
- 1365-2141
- OpenAlex
- W2089333962
- Cited by
- 80
- References
- 48
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 3 · 2023: 2 · 2022: 3 · 2021: 1 · 2020: 2 · 2019: 1 · 2018: 1 · 2017: 5 · 2016: 1 · 2015: 5 · 2014: 1 · 2013: 4 · 2012: 3
- FWCI
- 6.10
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- British Journal of Haematology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Cooley's Anemia Foundation
- Topics
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Health Sciences › Medicine › Genetics › Hemoglobinopathies and Related Disorders
- Life Sciences › Neuroscience › Neurology › Neurological diseases and metabolism
- Keywords
- hepcidin, beta-thalassemia, iron overload, iron metabolism, HepG2 cells, neutrophil gelatinase-associated lipocalin, hemochromatosis, transferrin saturation, serum factors, intestinal iron absorption
- MeSH terms
- Hemochromatosis Protein, Lipocalin-2, Acute-Phase Proteins, Blood Transfusion, Cell Line, Hemochromatosis, Humans, Membrane Proteins, Proto-Oncogene Proteins, Down-Regulation, Polymerase Chain Reaction, beta-Thalassemia, Hepatocytes, Antimicrobial Cationic Peptides, Lipocalins, GPI-Linked Proteins, Hepcidins
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