Peculiarities of placental microRNA expression in patients with preeclampsia and fetal growth restriction

Objective. To study the molecular mechanisms of fetal growth restriction and preeclampsia de-velopment based on a comparative analysis of the placental microRNA expression profile. Materials and methods. The study included 60 patients: Group 1 included 20 pregnant women with preeclampsia (PE) (main group), Group 2 (comparison group) included 20 pregnant women with fetal growth retardation (FGR), Group 3 included 20 healthy women with uncomplicated pregnancy and timely delivery (control group). All patients underwent general clinical, laboratory and instrumental studies, and the expression of 15 microRNAs in placental tissue was deter-mined: hsa-miR-20a-5p, hsa-miR-143-3p, hsa-miR-146a-5p, hsa-miR-181a-5p, hsa-miR-210-3p, hsa-miR-320a-3p, hsa-miR-375-3p, hsa-miR-517a-3p, hsa-miR-517c-3p, hsa-miR-574-3p, hsa-miR-574-5p, hsa-miR-1304-5p, hsa-miR-210-5p, hsa-miR-4498, hsa-miR-1972. Statistical data processing was performed using the licensed software package SPSS 26 and Statistica 12. Results. In the group with PE, compared with the control group, a statistically significant 10-fold decrease in the expression of microRNA hsa-miR-4498 (FC=0.11; p=0.04) and its increase in microRNA hsa-miR-20a-5p, hsa-miR-143-3p, hsa-miR-146a-5p (p≤0.05) were revealed. In the comparison group, the expression of hsa-miR-210-5p, hsa-miR-574-3p, hsa-miR-1972 was statistically significantly reduced compared with these indicators in the control group. In the main group, a statistically significant decrease in 5 microRNAs (hsa-miR-20a-5p, hsa-miR-143-3p, hsa-miR-210-5p, hsa-miR-574-3p, hsa-miR-1972) was recorded relative to the comparison group. With the development of PE in combination with FGR, a statistically significant decrease in the expression of 6 microRNAs (hsa-miR-146a-5p, hsa-miR-181a-5p, hsa-miR-210-5p, hsa-miR-320a-3p, hsa-miR-574-5p, hsa-miR-4498) was recorded compared to that in PE without fetal growth retardation. When comparing the levels of placental microRNAs in patients with moder-ate and severe PE, no statistically significant difference in microRNA expression among the ana-lyzed molecules was revealed. Conclusion. Pregnant women with PE and fetal growth retardation, compared to patients with physiological pregnancy, have a clear dysregulation of a number of placental microRNAs, which are potential regulators of many signaling pathways and biological processes (cell cycle, embryo-genesis, carcinogenesis, infectious and inflammatory processes, response to hypoxia, immune dysregulation, antiangiogenic and proinflammatory state). The obtained results confirm the muti-directionality of the etiopathogenetic links in the development of PE and IGR and similar final mechanisms for the development of early and late PE at the stage of clinical manifestations.