Go to JCI Insight
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Publication alerts by email
  • Advertising
  • Job board
  • Contact
  • Clinical Research and Public Health
  • Current issue
  • Past issues
  • By specialty
    • COVID-19
    • Cardiology
    • Gastroenterology
    • Immunology
    • Metabolism
    • Nephrology
    • Neuroscience
    • Oncology
    • Pulmonology
    • Vascular biology
    • All ...
  • Videos
    • Conversations with Giants in Medicine
    • Video Abstracts
  • Reviews
    • View all reviews ...
    • Complement Biology and Therapeutics (May 2025)
    • Evolving insights into MASLD and MASH pathogenesis and treatment (Apr 2025)
    • Microbiome in Health and Disease (Feb 2025)
    • Substance Use Disorders (Oct 2024)
    • Clonal Hematopoiesis (Oct 2024)
    • Sex Differences in Medicine (Sep 2024)
    • Vascular Malformations (Apr 2024)
    • View all review series ...
  • Viewpoint
  • Collections
    • In-Press Preview
    • Clinical Research and Public Health
    • Research Letters
    • Letters to the Editor
    • Editorials
    • Commentaries
    • Editor's notes
    • Reviews
    • Viewpoints
    • 100th anniversary
    • Top read articles

  • Current issue
  • Past issues
  • Specialties
  • Reviews
  • Review series
  • Conversations with Giants in Medicine
  • Video Abstracts
  • In-Press Preview
  • Clinical Research and Public Health
  • Research Letters
  • Letters to the Editor
  • Editorials
  • Commentaries
  • Editor's notes
  • Reviews
  • Viewpoints
  • 100th anniversary
  • Top read articles
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Publication alerts by email
  • Advertising
  • Job board
  • Contact
Top
  • View PDF
  • Download citation information
  • Send a comment
  • Terms of use
  • Standard abbreviations
  • Need help? Email the journal
  • Top
  • Version history
  • Article usage
  • Citations to this article

Advertisement

Corrigendum Free access | 10.1172/JCI63977

Hepcidin mediates transcriptional changes that modulate acute cytokine-induced inflammatory responses in mice

Ivana De Domenico, Tian Y. Zhang, Curry L. Koening, Ryan W. Branch, Nyall London, Eric Lo, Raymond A. Daynes, James P. Kushner, Dean Li, Diane M. Ward, and Jerry Kaplan

Find articles by De Domenico, I. in: PubMed | Google Scholar

Find articles by Zhang, T. in: PubMed | Google Scholar

Find articles by Koening, C. in: PubMed | Google Scholar

Find articles by Branch, R. in: PubMed | Google Scholar

Find articles by London, N. in: PubMed | Google Scholar

Find articles by Lo, E. in: PubMed | Google Scholar

Find articles by Daynes, R. in: PubMed | Google Scholar

Find articles by Kushner, J. in: PubMed | Google Scholar

Find articles by Li, D. in: PubMed | Google Scholar

Find articles by Ward, D. in: PubMed | Google Scholar

Find articles by Kaplan, J. in: PubMed | Google Scholar

Published June 1, 2012 - More info

Published in Volume 122, Issue 6 on June 1, 2012
J Clin Invest. 2012;122(6):2326–2326. https://doi.org/10.1172/JCI63977.
© 2012 The American Society for Clinical Investigation
Published June 1, 2012 - Version history
View PDF

Related article:

Hepcidin mediates transcriptional changes that modulate acute cytokine-induced inflammatory responses in mice
Ivana De Domenico, … , Diane M. Ward, Jerry Kaplan
Ivana De Domenico, … , Diane M. Ward, Jerry Kaplan
Research Article Inflammation

Hepcidin mediates transcriptional changes that modulate acute cytokine-induced inflammatory responses in mice

  • Text
  • PDF
Abstract

Hepcidin is a peptide hormone that regulates iron homeostasis and acts as an antimicrobial peptide. It is expressed and secreted by a variety of cell types in response to iron loading and inflammation. Hepcidin mediates iron homeostasis by binding to the iron exporter ferroportin, inducing its internalization and degradation via activation of the protein kinase Jak2 and the subsequent phosphorylation of ferroportin. Here we have shown that hepcidin-activated Jak2 also phosphorylates the transcription factor Stat3, resulting in a transcriptional response. Hepcidin treatment of ferroportin-expressing mouse macrophages showed changes in mRNA expression levels of a wide variety of genes. The changes in transcript levels for half of these genes were a direct effect of hepcidin, as shown by cycloheximide insensitivity, and dependent on the presence of Stat3. Hepcidin-mediated transcriptional changes modulated LPS-induced transcription in both cultured macrophages and in vivo mouse models, as demonstrated by suppression of IL-6 and TNF-α transcript and secreted protein. Hepcidin-mediated transcription in mice also suppressed toxicity and morbidity due to single doses of LPS, poly(I:C), and turpentine, which is used to model chronic inflammatory disease. Most notably, we demonstrated that hepcidin pretreatment protected mice from a lethal dose of LPS and that hepcidin-knockout mice could be rescued from LPS toxicity by injection of hepcidin. The results of our study suggest a new function for hepcidin in modulating acute inflammatory responses.

Authors

Ivana De Domenico, Tian Y. Zhang, Curry L. Koening, Ryan W. Branch, Nyall London, Eric Lo, Raymond A. Daynes, James P. Kushner, Dean Li, Diane M. Ward, Jerry Kaplan

×

Original citation: J. Clin. Invest. 2010;120(7): 2395–2405. doi:10.1172/JCI42011.

Citation for this corrigendum: J. Clin. Invest. 2012;122(6):2326. doi:10.1172/JCI63977.

The anti-Fpn and anti-Jak2 rows in Figure 2A were reprinted from I. De Domenico et al. (ref. 10) without attribution. They represent the same rows as were present in Figure 3B of that manuscript.

The authors regret the error.

Version history
  • Version 1 (June 1, 2012): No description

Article tools

  • View PDF
  • Download citation information
  • Send a comment
  • Terms of use
  • Standard abbreviations
  • Need help? Email the journal

Metrics

  • Article usage
  • Citations to this article

Go to

  • Top
  • Version history
Advertisement
Advertisement

Copyright © 2025 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)

Sign up for email alerts