[Analysis of metabolic pathways in intrauterine growth restriction]. / Analiz metabolicheskikh putei pri zaderzhke rosta ploda.

Objective was to analyze metabolic pathways based on a study of the metabolomic profile of pregnant women with intrauterine growth restriction. The metabolic profile of pregnant women with fetal growth restriction has been analyzed using liquid chromatography-mass spectrometry. At the second stage pathways were identified using SMPDB and MetaboAnalyst databases to clarify the relationship between metabolites. Biological networks allow to determine the effect of proteins on the metabolic pathways involved in pathogenesis of IUGR and determine the epigenetic mechanisms of its formation.

Enhanced Expression of TLR8 in Placental Tissue in Preeclampsia.

The expression of TLR8 in the placental tissue was studied in specimens from women of reproductive age with early- and late-onset preeclampsia (12 and 8 patients, respectively). The reference groups included 15 women: 10 with uneventful full-term pregnancy and 5 with preterm operative delivery on gestation weeks 28-33. The expression of TLR8 in placental structures was maximum in early-onset preeclampsia (p<0.01) characterized by the gravest clinical course, while the expression of TLR8 in late-onset preeclampsia was comparable with that in full-term pregnancy. This significant increase of TLR8 expression in placental tissue seemed to reflect activation of the key proinflammatory factors of congenital immunity and induction of the systemic inflammatory response. Manifest differences in the expression of TLR8 in late- and early-onset preeclampsia confirmed the hypothesis on different variants of this condition.

Peculiarities of RIG-1 Expression in Placental Villi in Preeclampsia.

The expression of RIG-1 in placenta samples was assessed in women of reproductive age with early- and late-onset preeclampsia and cesarean delivery at 27-39 weeks of gestation. The highest expression of RIG-1 was found in the syncytiotrophoblast of placental villi in the group with uncomplicated full-term pregnancy (normal); RIG-1 expression in groups with early- and late-onset preeclampsia was significantly (p<0.01) lower. In decidual cells, RIG-1 expression was also maximum in normal pregnancy and significantly (p<0.01) lower in lateonset preeclampsia. In the endothelium of villous capillaries, the maximum expression was observed in normal full-term pregnancy and in late-onset preeclampsia, while in early-onset preeclampsia this parameter was significantly (p<0.01) lower. It can be assumed that different variants of preeclampsia are mediated by similar pathogenetic mechanisms, including those related to immature molecular profile of the trophoblast and decidual cells, probably due to impaired stem cell activity in the placenta determining higher vulnerability and reduced regeneration capacity of the placental tissue. This is due to the fact that RIG-1 is one of the important signaling molecules that promote activation of stem cell and tissue regeneration.