State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing 100085, China.
University of Chinese Academy of Sciences, Beijing 100049, China.
Dis Markers. 2022 Aug 22;2022:1664474. doi: 10.1155/2022/1664474. eCollection 2022.
Increasing evidence reveals that iron deficiency during pregnancy causes adverse pregnancy outcomes. Thus far, the mechanisms underlying iron deficiency-associated preterm birth are mostly limited to animal studies. Whether the suggested mechanisms exist in human requires further investigation. The goal of this study was to characterize the iron metabolism in both the maternal side and fetal side in pregnant women with preterm birth.
Serum and placenta samples were collected from 42 pregnant women divided into four groups according to the gestational week. Indicators of iron metabolism, including serum iron, serum hepcidin, placental tissue iron, ferroportin (FPN), transferrin receptor 1 (TfR1), and ferritin, were surveyed using enzyme-linked immunosorbent assays (Elisa), Western blots, and real-time quantitative polymerase chain reactions (qRT-PCR).
Significant reduction of maternal serum iron was observed in women with preterm birth relative to those with full-term birth, indicative of worsen iron deficiency in those mothers with preterm birth. Meanwhile, the maternal hepcidin levels were notably diminished in women with preterm birth, whereas the fetal hepcidin levels were comparable between the two groups. Moreover, the placental iron stores were remarkably reduced in the preterm group, associated with reduced concentration of TfR1 and increased FPN concentration relative to the normal controls. In other words, the ratio of placental FPN mass to TfR1 mass (PIDI index) was strikingly increased in the preterm group.
Dysregulated iron homeostasis in both the maternal and fetal sides was implicated in preterm births, and disordered regulations in maintaining the placental iron equilibrium were also presumed to account for the compromised fetal iron supply.
越来越多的证据表明，孕妇铁缺乏会导致不良的妊娠结局。迄今为止，与缺铁相关的早产的机制大多局限于动物研究。这些机制是否存在于人类中还需要进一步研究。本研究的目的是描述早产孕妇母胎铁代谢的特点。
收集了 42 名孕妇的血清和胎盘样本，根据孕周分为四组。采用酶联免疫吸附试验（ELISA）、Western blot 和实时定量聚合酶链反应（qRT-PCR）检测血清铁、血清hepcidin、胎盘组织铁、铁蛋白（FPN）、转铁蛋白受体 1（TfR1）和 ferritin 等铁代谢指标。
与足月分娩的孕妇相比，早产孕妇的血清铁明显减少，表明这些孕妇的铁缺乏程度加重。同时，早产孕妇的血清 hepcidin 水平明显降低，而两组胎儿的 hepcidin 水平无差异。此外，早产组胎盘铁储存明显减少，TfR1 浓度降低，FPN 浓度升高，与正常对照组相比，胎盘 FPN 质量与 TfR1 质量的比值（PIDI 指数）显著增加。
母胎铁稳态失调与早产有关，胎盘铁平衡的调节紊乱也可能导致胎儿铁供应不足。
