原癌基因 GDF15、亚铁整合蛋白 1 和铁调素在真性红细胞增多症和原发性血小板增多症患者铁代谢中的作用。
The role of hepcidin, GDF15, and mitoferrin-1 in iron metabolism of polycythemia vera and essential thrombocytosis patients.
出版信息
Turk J Med Sci. 2019 Feb 11;49(1):74-80. doi: 10.3906/sag-1803-13.
BACKGROUND/AIM: GDF15, hepcidin and mitoferrin-1 (mfrn-1) are proteins involved in systemic iron regulation. There are no studies in the literature demonstrating the serum mfrn-1 levels in polycythemia vera (PV) and essential thrombocythemia (ET) patients. The aim of this study was to investigate GDF15, hepcidin and mfrn-1 levels in PV and ET patients.
MATERIALS AND METHODS
Ten PV, 17 ET patients, and 27 healthy controls (HCs) were enrolled. GDF15, hepcidin and mfrn-1 values were measured with enzyme-linked immunosorbent assay (ELISA).
RESULTS
GDF15 levels were higher in the myeloproliferative neoplasm (MPN) group (P = 0.002). Hepcidin levels were not different between MPN patients and HCs. The mfrn-1 levels were lower in MPN patients (P = 0.039). Hepcidin, GDF15, and mfrn-1 levels were not different between PV and ET patients. mfrn-1 levels were lower in ET patients than HCs (P = 0.038).
CONCLUSION
Increased erythropoiesis in MPNs may lead to high GDF15 levels in these patients. However, hepcidin was not suppressed despite the increased GDF15 levels and erythropoiesis in these patients. Decrease in mfrn-1 in MPNs can be the result of its increased turnover due to increased myelopoiesis. It can be hypothesized that similar hepcidin levels in patients and controls and low mfrn-1 levels in patients may be a defense mechanism against erythroid activity and thromboembolic complications.
背景/目的：GDF15、hepcidin 和 mitoferrin-1（mfrn-1）是参与全身铁调节的蛋白质。目前文献中尚无研究表明 GDF15 在真性红细胞增多症（PV）和原发性血小板增多症（ET）患者中的血清 mfrn-1 水平。本研究旨在探讨 PV 和 ET 患者的 GDF15、hepcidin 和 mfrn-1 水平。
材料和方法
纳入 10 例 PV、17 例 ET 患者和 27 例健康对照者（HCs）。采用酶联免疫吸附试验（ELISA）检测 GDF15、hepcidin 和 mfrn-1 值。
结果
MPN 组 GDF15 水平较高（P=0.002）。MPN 患者与 HCs 之间的 hepcidin 水平无差异。MPN 患者的 mfrn-1 水平较低（P=0.039）。PV 和 ET 患者之间的 hepcidin、GDF15 和 mfrn-1 水平无差异。ET 患者的 mfrn-1 水平低于 HCs（P=0.038）。
结论
MPNs 中红细胞生成增加可能导致这些患者的 GDF15 水平升高。然而，尽管这些患者的 GDF15 水平和红细胞生成增加，但 hepcidin 并未受到抑制。MPNs 中 mfrn-1 的减少可能是由于其髓系细胞增生增加导致的周转率增加所致。可以假设，患者和对照组中相似的 hepcidin 水平和患者中较低的 mfrn-1 水平可能是针对红细胞生成活性和血栓栓塞并发症的防御机制。
Zotero 插件