کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5913323 | 1570399 | 2016 | 27 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Characterization of hepcidin response to holotransferrin in novel recombinant TfR1 HepG2 cells
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موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شناسی مولکولی
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
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.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Blood Cells, Molecules, and Diseases - Volume 61, October 2016, Pages 37-45
Journal: Blood Cells, Molecules, and Diseases - Volume 61, October 2016, Pages 37-45
نویسندگان
Kosha Mehta, Mark Busbridge, Derek Renshaw, Robert W. Evans, Sebastien Farnaud, Vinood B. Patel,