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Blood, 1 November 2006, Vol. 108, No. 9, pp. 3204-3209. Prepublished online as a Blood First Edition Paper on July 11, 2006; DOI 10.1182/blood-2006-06-027631. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2006-06-027631v1 108/9/3204    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Wrighting, D. M. Articles by Andrews, N. C. Search for Related Content PubMed PubMed Citation Articles by Wrighting, D. M. Articles by Andrews, N. C. Related Collections Immunobiology Red Cells Signal Transduction Free Research Articles Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  RED CELLS Interleukin-6 induces hepcidin expression through STAT3 Diedra M. Wrighting, and Nancy C. Andrews From the graduate program in Biological and Biomedical Sciences, Harvard University, Boston, MA; the Division of Hematology/Oncology, Children's Hospital Boston and the Department of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA; and the Howard Hughes Medical Institute, Chevy Chase, MD. Iron homeostasis is maintained through meticulous regulation of circulating hepcidin levels. Hepcidin levels that are inappropriately low or high result in iron overload or iron deficiency, respectively. Although hypoxia, erythroid demand, iron, and inflammation are all known to influence hepcidin expression, the mechanisms responsible are not well defined. In this report we show that the inflammatory cytokine interleukin-6 (IL-6) directly regulates hepcidin through induction and subsequent promoter binding of signal transducer and activator of transcription 3 (STAT3). STAT3 is necessary and sufficient for the IL-6 responsiveness of the hepcidin promoter. Our findings provide a mechanism by which hepcidin can be regulated by inflammation or, in the absence of inflammatory stimuli, by alternative mechanisms leading to STAT3 activation. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Regulating the master iron regulator hepcidin Chaim Hershko Blood 2006 108: 2890-2891. [Full Text] [PDF] This article has been cited by other articles: P. Matak, T. B. Chaston, B. Chung, S. K. Srai, A. T. McKie, and P. A. Sharp Activated macrophages induce hepcidin expression in HuH7 hepatoma cells Haematologica, June 1, 2009; 94(6): 773 - 780. [Abstract] [Full Text] [PDF] H. Huang, M. 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