Iron regulation of transferrin synthesis in the human hepatoma cell line HepG2
Iron regulation of transferrin synthesis in the human hepatoma cell line HepG2
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DOI：
10.1006/cbir.1999.0456
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发表时间：
2000-01-01
影响因子：
3.9
通讯作者：
Adrian, GS
中科院分区：
文献类型：
--
作者：
Barnum-Huckins, K;Adrian, GS
在人类中，血清转铁蛋白水平在铁缺乏时升高，并在铁过载时降低。然而，铁水平是否实际上影响人肝细胞中转铁蛋白的合成尚不清楚。在之前的研究中，铁被证明可以抑制转基因小鼠肝脏中嵌合人转铁蛋白基因的表达。本研究的目的是通过测试铁水平变化对人肝癌细胞系 HepG2 中转铁蛋白合成的影响，确定铁是否会抑制完整的内源性人转铁蛋白合成。在 HepG2 细胞中，用氯高铁血红素或柠檬酸铁处理后，标准化的 S-35 代谢标记转铁蛋白合成始终低于用铁螯合剂去铁胺处理后的情况。因此，这项研究提供了新的证据，证明铁可以调节完整内源性人转铁蛋白的合成。 (C) 2000 年学术出版社。
In human beings, serum transferrin levels increase during iron deficiency and decrease with iron overload. Yet, whether or not iron levels actually affect the synthesis of transferrin in human liver cells is not known. In previous studies, iron was shown to suppress the expression of chimeric human transferrin genes in livers of transgenic mice. The goal of this study was to determine if iron suppresses intact endogenous human transferrin synthesis by testing the effects of changes in iron levels on synthesis of transferrin in a human hepatoma cell line HepG2. In HepG2 cells, normalized S-35-metabolically labeled transferrin synthesis was consistently less following iron treatment with hemin or ferric citrate, than following treatment with an iron-chelator deferroxamine. Thus, this study provides new evidence that iron can regulate synthesis of intact endogenous human transferrin. (C) 2000 Academic Press.