Erythropoietin's inhibiting impact on hepcidin expression occurs indirectly
Open accessAbstract
Under conditions of accelerated erythropoiesis, elevated erythropoietin (Epo) levels are associated with inhibition of hepcidin synthesis, a response that ultimately increases iron availability to meet the enhanced iron needs of erythropoietic cells. In the search for erythroid regulators of hepcidin, many candidates have been proposed, including Epo itself. We aimed to test whether direct interaction between Epo and the liver is required to regulate hepcidin. We found that prolonged administration of high doses of Epo in mice leads to great inhibition of liver hepcidin mRNA levels, and concomitant induction of the hepcidin inhibitor erythroferrone (ERFE). Epo treatment also resulted in liver iron mobilization, mediated by increased ferroportin activity and accompanied by reduced ferritin levels and increased TfR1 expression. The same inhibitory effect was observed in mice that do not express the homodimeric Epo receptor (EpoR) in liver cells because EpoR expression is restricted to erythroid cells. Similarly, liver signaling pathways involved in hepcidin regulation were not influenced by the presence or absence of hepatic EpoR. Moreover, Epo analogs, possibly interacting with the postulated heterodimeric β common EpoR, did not affect hepcidin expression. These findings were supported by the lack of inhibition on hepcidin found in hepatoma cells exposed to various concentrations of Epo for different periods of times. Our results demonstrate that hepcidin suppression does not require the direct binding of Epo to its liver receptors and rather suggest that the role of Epo is to stimulate the synthesis of the erythroid regulator ERFE in erythroblasts, which ultimately downregulates hepcidin.
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EPO itself can reduce hepcidin production via inhibition of the BMP-SMAD pathway.
“Indeed, EPO itself can reduce hepcidin production via inhibition of the BMP-SMAD pathway (Gammella et al., 2015)”
From The Role of Iron Regulation in Immunometabolism and Immune-Related Disease (2019) · cites this paper as Gammella et al., 2015
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- Authors
- Gammella, E., Diaz, V., Recalcati, S., Buratti, P., Samaja, M., Dey, S., Noguchi, C. T., Gassmann, M., & Cairo, G.
- Affiliations
- University of Milan (IT)
- Institute of Veterinary Physiology, Vetsuisse Faculty, and Zurich Center for Integrative Human Physiology, University of Zurich, Zurich, Switzerland;
- National Institutes of Health (US)
- Universidad Peruana Cayetano Heredia (PE)
- Corresponding author
- Cairo, Gaetano
- ORCID
- Venue
- American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
- Publisher
- American Physiological Society
- Published
- 2015-02-15
- Volume
- 308
- Issue
- 4
- Pages
- R330-R335
- ISSN
- 0363-6119 (ISSN-L)
- 1522-1490
- PMC
- PMC4347750
- OpenAlex
- W2112234535
- Cited by
- 59
- References
- 25
- Citations by year
- 2025: 2 · 2024: 3 · 2023: 6 · 2022: 6 · 2021: 6 · 2020: 2 · 2019: 7 · 2018: 7 · 2017: 6 · 2016: 8 · 2015: 6
- FWCI
- 4.73
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- American Journal of Physiology-Regulatory, Integrative and Comparative Physiology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Zurich Open Repository and Archive (University of Zurich) (acceptedVersion)
- Archivio Istituzionale della Ricerca (Universita Degli Studi Di Milano) (submittedVersion, other-oa)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion)
- Zurich Open Repository and Archive (University of Zurich)
- Topics
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Health Sciences › Medicine › Hematology › Erythropoietin and Anemia Treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Hemoglobin structure and function
- Keywords
- erythropoietin, hepcidin, erythroferrone, erythropoietin receptor, ferroportin, ferritin, transferrin receptor 1, iron homeostasis, erythropoiesis, erythroid cells, hepatoma cells
- MeSH terms
- Animals, Dose-Response Relationship, Drug, Erythropoietin, Humans, Iron, Liver, Male, Mice, Inbred C57BL, Mice, Inbred ICR, Muscle Proteins, Oligopeptides, RNA, Messenger, Time Factors, Down-Regulation, Cytokines, Receptors, Erythropoietin, Mice, Knockout, Hep G2 Cells, Hepcidins
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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