[Morphological markers of mitochondrial dysfunction of the basal plate cytotrophoblast of the placenta in preeclampsia of varying severity].

Pathomorphological changes in preeclampsia develop in all elements of the functional system "mother-placenta-fetus" and play a leading role in the course and outcome of pregnancy.

Objective: To identify morphological markers of mitochondrial dysfunction of the basal plate cytotrophoblast of the placenta in women with preeclampsia of varying severity.

Material and methods: Comprehensive morphological examination of placentas from women with uncomplicated pregnancy (30), moderate (30) and severe (30) preeclampsia included overview histology, morphometry, immunohistochemistry and transmission electron microscopy.

Results: Regardless of the severity of preeclampsia, a leading place in the pathomorphological change in the placenta is occupied by a violation of uteroplacental circulation due to a violation of cytotrophoblast invasion. Immunohistochemical parameters of mitochondrial dysfunction of cytotrophoblast cells of the basal lamina have been determined. A significant decrease in the expression of mtDNA transcription and replication proteins (TFAM, POLG) and a violation of the structure of the respiratory chain (NADH+, cytochrome C) were revealed. These changes were combined with ultrastructural rearrangement of mitochondria, which are the basis of ATP synthesis. In moderate preeclampsia, a decrease in the number of mitochondria was revealed, the ratio of oval and rounded forms of mitochondria associated with swelling of the central parts of the crist changes. In severe preeclampsia, the structural basis of the connection of energy metabolism between mitochondria and the granular endoplasmic reticulum is interrupted. The progressive destruction of mitochondrial crysts with the formation of pseudovesicles ends with total necrosis of ultrastructures.

Conclusion: In pregnant women with preeclampsia, mitochondrial dysfunction of the cytotrophoblast cells of the basal lamina was diagnosed, characterized by a decrease in the expression of mtDNA transcription and replication proteins in combination with a violation of the I-III enzymatic complexes of the respiratory chain. The identified immunohistochemical markers are pathogenetically associated with ultrastructural rearrangement of mitochondria in preeclampsia of varying severity.