ИСТИНА

Among different pathologies, associated with mitochondrial dysfunction preeclampsia (PE) is a pregnancy-specific syndrome, characterizing by hypertension, proteinuria, and other systemic disturbances. Preeclampsia affects 2–8% of pregnancies and it is still the major cause of maternal and fetal morbidity and mortality worldwide. The main features of PE are decreasing of trophoblast invasion and abnormal remodeling of spiral arteries in myometrium layer caused by malfunctioning of mitochondrion. In present work we study both myometrium and placenta tissue from women with normal pregnancy, patients with late- and earlyonset PE because we proposed bidirectional signal transduction in a systemmother- placenta-fetus. Methods: Mitochondria isolation, oxygen consumption, ROS production rate and membrane potential determination, fluorescent confocal microscopy, qPCR-RT, SDS-PAAG, WB, statistics. Results: we found significant changes in content of antioxidant enzymes, markers of mitochondrial biogenesis and autophagy proteins in preeclamptic myometrium. Levels of superoxide dismutase and catalase were down-regulated in both groups with PE. In late-onset PE we found up-regulation of VDAC1 and TFAM as well as PGC-1 alpha and PGC- 1-beta. In placenta tissue we observed significant decrease of TFAM level and upraise of OPA1 level and mtDNA copy number in early-onset PE group. On isolated mitochondria we found that P/O ratio, parameter of respiration efficiency, was also increased in both PE groups. These findings suggest about crucial molecular changes, which occur in maternal myometrium and placenta developing preeclampsia. Conclusion: we proposed placenta influence to maternal organism through the extracellular messengers like ROS, Ca2+ and microparticles, circulating in mother’s blood at preeclampsia. Alterations in protein’s level, observed in our study, could be explained by the impact of mentioned agents derived from placenta.