Fetal liver hepcidin secures iron stores in utero
Open accessPublished version of a preprint
Abstract
In the adult, the liver-derived hormone hepcidin (HAMP) controls systemic iron levels by blocking the iron-exporting protein ferroportin (FPN) in the gut and spleen, the sites of iron absorption and recycling, respectively. Impaired HAMP expression or FPN responsiveness to HAMP result in iron overload. HAMP is also expressed in the fetal liver but its role in controlling fetal iron stores is not understood. To address this question in a manner that safeguards against the confounding effects of altered maternal iron homeostasis, we generated fetuses harboring a paternally-inherited ubiquitous knock-in of the HAMP-resistant fpnC326Y. Additionally, to safeguard against any confounding effects of altered placental iron homeostasis, we generated fetuses with a liver-specific knock-in of fpnC326Y or knockout of the hamp gene. These fetuses had reduced liver iron stores and hemoglobin, and markedly increased FPN in the liver, but not in the placenta. Thus, fetal liver HAMP operates cell-autonomously to increase fetal liver iron stores. Our findings also suggest that FPN in the placenta is not actively regulated by fetal liver HAMP under normal physiological conditions.
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Iron retained in the fetal liver by fetal hepcidin is used for fetal erythropoiesis until erythropoiesis transitions to the marrow, close to birth.
“where it is used for fetal erythropoiesis until erythropoiesis transitions to the marrow, close to birth.”
From Hepcidin-Ferroportin Interaction Controls Systemic Iron Homeostasis (2021) · cites this paper as [51]
Fetal hepatic production of hepcidin may be sufficient to act on fetal hepatic ferroportin in an autocrine/paracrine manner to retain iron in the fetal liver.
“However, fetal hepatic production of hepcidin may be sufficient to act on fetal hepatic ferroportin in an autocrine/paracrine manner to retain iron in the fetal liver [51]”
From Hepcidin-Ferroportin Interaction Controls Systemic Iron Homeostasis (2021) · cites this paper as [51]
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- Authors
- Kämmerer, L., Mohammad, G., Wolna, M., Robbins, P. A., & Lakhal-Littleton, S.
- Affiliations
- University of Oxford (GB)
- Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford, United Kingdom
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2020-09-24
- Volume
- 136
- Issue
- 13
- Pages
- 1549-1557
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- PMC
- PMC7515687
- OpenAlex
- W3031036471
- Cited by
- 38
- References
- 41
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 5 · 2023: 4 · 2022: 9 · 2021: 9 · 2020: 2
- FWCI
- 3.79
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Blood (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- British Heart Foundation (FS/12/63/29895)
- Medical Research Council (MR/L010054/1)
- Topics
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Health Sciences › Nursing › Nutrition and Dietetics › Trace Elements in Health
- Life Sciences › Neuroscience › Neurology › Neurological diseases and metabolism
- Keywords
- hepcidin, fetal liver, iron stores, ferroportin, iron homeostasis, hemoglobin
- MeSH terms
- Ferroportin, Animals, Female, Hemoglobins, Iron, Liver, Male, Pregnancy, Cation Transport Proteins, Mice, Hepcidins
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