ИСТИНА

Preeclampsia (PE) is a pregnancy-specific syndrome, characterizing by hypertension, proteinuria, and other systemic disturbances. Pre-eclampsia affects 2–8% of all pregnancies and it is still the major cause of maternal and fetal morbidity and mortality worldwide. The main morphological aspects of PE are poor trophoblast invasion and abnormal remodeling of spiral arteries. Placenta insufficiency on the tissue and cell level may be associated with defects in trophoblast mitochondrial morphology and functionality as a biomarker of oxidative stress related disorders. Purpose of this work was a study of mitochondrial structure and functionality in early- and late-onset preeclampsia. In our work we collected placental samples after delivery via cesarean section and divided them into three groups: control group (n = 14), early- and late-onset preeclampsia (n = 13, n = 12, respectively). We investigated the relative expression level of genes and proteins, responsible for biogenesis, activation of mtDNA transcription and certain mitochondrial structure proteins(MFN1,MFN2,OPA1,VDAC1,TFAM). Also we determined the signifcant difference in mtDNA copy number between PEs and control groups and in markers, which are essential for normal mitochondrial morphology and function. In early-onset PE we observed low calcium capacity and increase of complex I respiratory efficiency. In both PE groups we obtained increase of P/O ratio. Early-onset PE is often severe and late-onset PE is often mild. Thus, in preterm PE mitochondrial molecular pathology is more pronounced and even not similar to late-onset one. We assume that the segregation of mitochondrial DNA occurs as a result of competition between TFAM and OPA1 and precedes the fission of mitochondria in order to select an intact mitochondrial DNA by quality control system at the stage of mitoplasts fragmentation rather than whole mitochondria. This work was supported by Russian Foundation for Basic Research with grant RFBR no. 14-04-01617A.