Abstract. To identify the specific serum preeclampsia (PE)-related biomarkers, 10 microRNAs (miRNAs) were selected based on their reported aberrant (4 upregulated and 6 downregulated) expression in PE placenta. A total of 1,035 pregnant patients were enrolled. Finally, 32 pregnancies with PE and 32 healthy pregnancies were incorporated in the study. The expression of these 10 miRNAs in the different trimesters was determined by SYBR-Green reverse transcription-quantitative polymerase chain reaction. Compared with that in the healthy controls, the expression levels of miR-152, miR-183 and miR-210 in PE serum were higher in the second and third trimester, whereas the expression of miR-182 was only higher in the third trimester. The expression levels of 6 miRNAs (miR-1, miR-328, miR-363, miR-377, miR-500 and miR-584) that were downregulated in PE placenta showed no significant differences between pregnancies complicated by PE and healthy pregnancies throughout the 3 trimesters. Areas under the receiver operating characteristic [standard error (SE)] during the 20-24th gestational week for predicting PE were 0.026), 0.031) and miR-210: 0.93 (SE, 0.018). In conclusion, the expression levels of serum miR-152, miR-183 and miR-210 were elevated since the second trimester in pregnancies complicated with PE, indicating their potentials as serum biomarkers for forecasting PE.

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The eicosanoids 11,12-EET, 5-HETE, 8-HETE, 12-HETE, 15-HETE, and leukotriene B4 might play important parts in the occurrence and development of pre-eclampsia.

During pregnancy, disorders in uterine spiral artery remodeling (USAR) cause preeclampsia and other diseases. The aim of this study was to investigate the effect of 20-hydroxyeicosatetraenoic acid (20-HETE) on the biological behavior of human villous trophoblasts (HVTs) and human uterine vascular smooth muscle cells (HUVSMCs), and explore the role of 20-HETE in USAR. 20-HETE and its inhibitor HET0016 were used to study migration, invasion and apoptosis in the HVT and HVT-HUVSMC models. 20-HETE inhibited the migration and invasion of HVTs, and inhibited apoptosis in HUVSMCs and HUVSMCs co-cultured with HVTs. 20-HETE had thus obvious effects on the biological behavior of HVTs and HUVSMCs. These effects may cause USAR disorders and vascular dysfunction, leading to preeclampsia.

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