4.0 Article

Characterization of hepcidin response to holotransferrin in novel recombinant TfR1 HepG2 cells

期刊

BLOOD CELLS MOLECULES AND DISEASES
卷 61, 期 -, 页码 37-45

出版社

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bcmd.2016.06.008

关键词

Hepcidin; Iron; HepG2; Hepatocyte; Transferrin

资金

  1. University of Westminster

向作者/读者索取更多资源

Hepcidin is the key regulator of systemic iron homeostasis. The iron-sensing mechanisms and the role of intracellular iron in modulating hepatic hepcidin secretion are unclear. Therefore, we created a novel cell line, recombinant-TfR1 HepG2, expressing iron-response-element-independent TFRC mRNA to promote cellular iron-overload and examined the effect of excess holotransferrin (5 g/L) on cell-surface TfR1, iron content, hepcidin secretion and mRNA expressions of TFRC, HAMP, SLC40A1, HFE and TFR2. Results showed that the recombinant cells exceeded levels of cell-surface TfR1 in wild-type cells under basal (2.8-fold; p < 0.03) and holotransferrin-supplemented conditions for 24 h and 48 h (4.4- and 7.5-fold, respectively; p < 0.01). Also, these cells showed higher intracellular iron content than wild-type cells under basal (3-fold; p < 0.03) and holotransferrin-supplemented conditions (6.6-fold at 4 h; p < 0.01). However, hepcidin secretion was not higher than wild-type cells. Moreover, holotransferrin treatment to recombinant cells did not elevate HAMP responses compared to untreated or wild-type cells. In conclusion, increased intracellular iron content in recombinant cells did not increase hepcidin responses compared to wild-type cells, resembling hemochromatosis. Furthermore, TFR2 expression altered within 4 h of treatment, while HFE expression altered later at 24 h and 48 h, suggesting that TFR2 may function prior to HFE in HAMP regulation. (C) 2016 The Authors. Published by Elsevier Inc.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.0
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据