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Hepcidin Induces M1 Macrophage Polarization in Monocytes or THP-1 Derived Macrophages | ||
Iranian Journal of Immunology | ||
مقاله 1، دوره 16، شماره 3، آذر 2019، صفحه 190-199 اصل مقاله (1.27 M) | ||
نوع مقاله: Original Article | ||
شناسه دیجیتال (DOI): 10.22034/iji.2019.80270 | ||
نویسندگان | ||
Enna Liu* 1؛ Zheng Li2؛ Yan Zhang1؛ Kuisheng Chen3 | ||
1Department of Tumor Pathology, Luohe Medical College, Henan, China | ||
2Yi-Chuang Institute of Biotechnology Industry, Beijing, China | ||
3College of Basic Medicine, Zhengzhou University, Henan, China | ||
چکیده | ||
Background: Macrophage polarization plays a critical role in determining the inflammatory states. Hepcidin is a key negative regulator of iron homeostasis and functions. Although hepcidin has been shown to affect ferroportin expression in macrophages, whether it affects macrophage polarization is still largely unknown. Objective: To address whether hepcidin induces macrophage polarization. Methods: The expression of iNOS and CD206, and the ratio of IFN-γ vs IL-4 in THP-1 derived macrophages upon hepcidin stimulation were evaluated. Further detected was the percentage of CD16+ M1, CD23+ M1, CD10+ M2 and CCL22+ M2 cells in monocyte derived macrophages. Results: M1 associated molecules were increased in hepcidin-treated cells, yet M2 associated molecules were increased when hepcidin was neutralized. Concomitantly, we observed a significant increase in IRF3 phosphorylation in hepcidin-stimulated cells. However, STAT6 phosphorylation with hepcidin was neutralized. Conclusion: Hepcidin is able to induce macrophage polarization towards M1 type, and might be utilized as a potential M1 macrophage agonist in clinical practice. | ||
کلیدواژهها | ||
Hepcidin؛ Macrophage؛ Polarization | ||
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