演題詳細

一般口演 / Oral Session

一般口演 1 (Oral Session 1) :鉄代謝 (Iron Metabolism)

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日程
2013年10月11日(金)
時間
09:30 - 10:30
会場
第3会場 / Room No.3 (さっぽろ芸文館 3F 蓬莱)
座長・司会
川端 浩 (Hiroshi Kawabata):1
1:京都大学 血液・腫瘍内科学
 
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The regulators of hepcidin under erythropoietic stimulation induced by C.E.R.A. administration

演題番号 : OS-1-5

松尾 有佳里 (Yukari Matsuo):1、佐々木 雄亮 (Yusuke Sasaki):1、野口 真理子 (Mariko Noguchi):1、萬 啓悟 (Keigo Yorozu):1、下中 靖 (Yasushi Shimonaka):1

1:Product Research Dept., Chugai Pharmaceutical Co., Ltd., Japan

 

Background and aims:Hepcidin is a key regulator of iron homeostasis. Although several candidates of hepcidin regulators have reported under hematopoietic stimulation, such as GDF15 and TWSG1, associations between hepcidin and these factors have not fully understood. We showed that Continuous Erythropoietin Receptor Activator (C.E.R.A.) enhanced hematopoiesis and iron metabolism through profound suppression of hepcidin. In this study, we examined the regulator of hepcidin under several conditions of C.E.R.A. administration.
Methods:C57BL/6N mice were intravenously injected with 1 or 2 μg/kg of C.E.R.A. on Day0 and 1 μg/kg of C.E.R.A. on Day7. Mice sera were collected on Day2, 5, 7, 9, 12 and 14 and hepcidin, GDF15, TWSG1 and other iron parameters were analyzed. We also analyzed the maturation of erythroblasts by flow cytometry, staining Ter119 and CD71.
Results:Until Day5, hepcidin was suppressed strongly by 2 μg/kg of C.E.R.A and moderately by 1 μg/kg of C.E.R.A. Mice injected with 1 μg/kg of C.E.R.A. on Day0 and 7 showed hepcidin suppression in a repetitive manner. Under these conditions, serum GDF15 levels, as well as TWSG1 and ferritin were not associated with hepcidin levels, but percentages of Ter119+CD71+ cells were closely related to hepcidin.
Conclusions:These results indicate that hepcidin is not regulated neither by GDF15, TWSG1 nor ferritin, but regulated by erythroid maturation-status under erythropoietic stimulation after C.E.R.A. administration, supporting the concept that hepcidin is controlled via iron demand of immature erythroblasts.

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