The Korea Institute for Public Sperm Bank, Busan 49241, Republic of Korea.
Department of Obstetrics and Gynecology, Pusan National University School of Medicine, Biomedical Research Institute, Busan 49241, Republic of Korea.
Mol Med Rep. 2018 Apr;17(4):5292-5299. doi: 10.3892/mmr.2018.8539. Epub 2018 Feb 1.
The mechanism underlying the pathogenesis of preeclampsia (PE) has been previously investigated but remains to be elucidated. Among numerous biomarkers that are associated with the pathogenesis of PE, leptin is most frequently investigated. Although studies concerning the association between PE and the expression of leptin in the serum and placenta have been conducted, the results are conflicting and inconsistent. Furthermore, the expression of leptin and its receptors in the placental bed and their association with PE, to the best of our knowledge, has not been previously reported. Therefore, to determine the association between the expression of leptin and its receptor, and pathogenesis and onset period of PE, placental bed tissues were obtained from cesarean section deliveries. The mRNA and protein expression levels of leptin and its receptor were investigated in normal pregnancies (n=18), pregnancies complicated with early‑onset PE (n=9) and late‑onset PE (n=9) by reverse transcription‑quantitative polymerase chain reaction and western blotting, respectively. The results demonstrated that the mRNA and protein expression of leptin in the placental bed was significantly increased in the PE groups compared with normal controls and was associated with the onset period of PE. Furthermore, as evidenced by immunostaining, leptin was upregulated in endothelial cells of the placental bed in the PE groups, with a particularly strong upregulation in activated endothelial cells from patients with early‑onset PE. The results of the present study indicate that altered expression of leptin in the placental bed may contribute to the pathogenesis of PE.
子痫前期（PE）发病机制的基础已被前人研究过，但仍有待阐明。在与 PE 发病机制相关的众多生物标志物中，瘦素是最常被研究的。虽然已有研究探讨了 PE 与血清和胎盘瘦素表达之间的关系，但结果相互矛盾，不一致。此外，据我们所知，瘦素及其受体在胎盘床中的表达及其与 PE 的关系尚未被报道。因此，为了确定瘦素及其受体的表达与 PE 的发病机制和发病时间之间的关系，从剖宫产术中获取胎盘床组织。通过逆转录-定量聚合酶链反应和 Western blot 分别检测正常妊娠（n=18）、早发型 PE（n=9）和晚发型 PE（n=9）患者中瘦素及其受体的 mRNA 和蛋白表达水平。结果表明，PE 组胎盘床中瘦素的 mRNA 和蛋白表达水平明显高于正常对照组，且与 PE 的发病时间有关。此外，免疫组化染色结果表明，PE 组胎盘床内皮细胞中的瘦素表达上调，早发型 PE 患者激活的内皮细胞中瘦素表达上调更为明显。本研究结果表明，胎盘床中瘦素表达的改变可能导致 PE 的发病机制。
