ArticleInternational journal of hematology2009
Oncostatin M and leukemia inhibitory factor increase hepcidin expression in hepatoma cell lines.
Article in International journal of hematology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 31 citations in OpenAlex.
- HFE-Related Hemochromatosis May Be a Primary Kupffer Cell Disease.Biomedicines · 2025Review
- Hepcidin Promoted Ferroptosis through Iron Metabolism which Is Associated with DMT1 Signaling Activation in Early Brain Injury following Subarachnoid Hemorrhage.Oxidative medicine and cellular longevity · 2021Article
- Recent insights into targeting the IL-6 cytokine family in inflammatory diseases and cancer.Nature reviews. Immunology · 2018Review
- High pretransplant hepcidin levels are associated with poor overall survival and delayed platelet engraftment after allogeneic hematopoietic stem cell transplantation.Cancer medicine · 2017Article
- Regulation of the Iron Homeostatic Hormone Hepcidin.Advances in nutrition (Bethesda, Md.) · 2017Review
- Oncostatin m modulation of lipid storage.Biology · 2015Review
- Article
- The enigmatic cytokine oncostatin m and roles in disease.ISRN inflammation · 2013Review
- Acidic milieu augments the expression of hepcidin, the central regulator of iron homeostasis.International journal of hematology · 2012Article
- LIF-dependent signaling: new pieces in the Lego.Stem cell reviews and reports · 2012Review
- A tincture of hepcidin cures all: the potential for hepcidin therapeutics.The Journal of clinical investigation · 2010Article
- Ferroportin and erythroid cells: an update.Advances in hematology · 2010Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Overproduction of hepcidin by interleukin-6 (IL-6) is considered to be the main factor responsible for the development of anemia in inflammatory conditions. Since oncostatin M (OSM), a member of the IL-6 family, plays an important role in immune and inflammatory responses, we assessed the effect of OSM on hepcidin expression, as well as that of leukemia inhibitory factor (LIF), another member of the IL-6 family. We found that hepcidin expression was markedly induced by OSM and LIF in a time- and dose-dependent manner in hepatoma cell lines, and this expression was induced independent of IL-6/IL-6 receptor signaling. Luciferase assay revealed that OSM and LIF stimulated a -1.3-kb hepcidin promoter. This effect was markedly reduced when the signal transducer and activator of transcription (STAT) site of the promoter was mutated, and was almost completely abolished in the presence of AG-490, a Janus kinase (JAK) inhibitor. Hence, the JAK/STAT pathway plays a major role in OSM- and LIF-induced activation of the hepcidin promoter. In conclusion, we demonstrated that OSM and LIF can induce hepcidin expression mainly through the JAK/STAT pathways. Further studies are warranted to evaluate the clinical significance of OSM and LIF in the development of anemia in various inflammatory diseases.
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