Jiang Liansheng, Long Anxiong, Tan Longyi, Hong Mao, Wu Jingjing, Cai Leiming, Li Qian
Department of Clinical Laboratory, Shanghai First People's Hospital Baoshan Branch, Shanghai, PR China.
Department of Obstetrics and Gynecology, Shanghai First People's Hospital Baoshan Branch, Shanghai, PR China.
Placenta. 2017 Mar;51:70-75. doi: 10.1016/j.placenta.2017.02.001. Epub 2017 Feb 2.
Pre-eclampsia (PE) is a common and severe obstetric complication. MicroRNAs (miRs) have emerged as molecules that are associated with the disease.
Quantitative reverse transcription PCR (RT-qPCR) was used for serum miR-520g characterization from 19 severe pre-eclamptic and 19 normal pregnancies. In situ hybridation was adopted to localize microRNA-520g (miR-520g). Migration and invasion of HTR-8/SVneo cells were evaluated after miR-520g mimic treatment with transwell system. MiR-520g target gene was verified in luciferase reporter system.
The expression of serum miR-520g displayed an upward trend as pregnancies progress. At first-trimester, miR-520g in pre-eclampsia was significantly higher than that in the control, but no significant differences were found in the second and last trimesters. MiR-520g localized in cytoplasm of early trimester placental trophoblasts. The migration and invasion of HTR8/SVneo were inhibited by miR-520g mimic treatment. Matrix metalloproteinase 2 (MMP2) was verified as a direct target of miR-520g.
Elevated maternal serum level of miR-520g level in first trimester was detected in patients with severe PE. By suppressing the migration and invasion of trophoblast via at least partial inhibition of MMP2 translation inhibition, miR-520g might play a role in the defective spiral artery remodeling, and thus contribute to pre-eclampsia pathophysiology.
子痫前期（PE）是一种常见且严重的产科并发症。微小RNA（miRs）已成为与该疾病相关的分子。
采用定量逆转录聚合酶链反应（RT-qPCR）对19例重度子痫前期孕妇和19例正常孕妇的血清miR-520g进行特征分析。采用原位杂交法对微小RNA-520g（miR-520g）进行定位。用transwell系统评估miR-520g模拟物处理后HTR-8/SVneo细胞的迁移和侵袭能力。在荧光素酶报告系统中验证miR-520g的靶基因。
随着孕期进展，血清miR-520g的表达呈上升趋势。在孕早期，子痫前期患者的miR-520g显著高于对照组，但在孕中期和晚期未发现显著差异。miR-520g定位于孕早期胎盘滋养层细胞胞质中。miR-520g模拟物处理可抑制HTR8/SVneo细胞的迁移和侵袭。基质金属蛋白酶2（MMP2）被验证为miR-520g的直接靶标。
重度子痫前期患者孕早期母体血清miR-520g水平升高。通过至少部分抑制MMP2翻译来抑制滋养层细胞的迁移和侵袭，miR-520g可能在螺旋动脉重塑缺陷中发挥作用，从而导致子痫前期的病理生理过程。
