INTRODUCTION
Fetal growth restriction (FGR) is a serious obstetric pathology that leads to high perinatal morbidity and mortality. Despite the large number of works on FGR, the mechanisms of its development are not sufficiently studied, which affects the effectiveness of therapy. Since fetal growth disorders largely depend on damage to placental functions, changes in metabolic processes in this organ, especially at the molecular level, can play a leading role in the development of FGR.
OBJECTIVE
To study posttranslational modifications of placental mitochondrial and cytoplasmic proteins in ZRP and assess their role in the formation of this pathology of pregnancy.
MATERIALS AND METHODS
The observational single-center, simultaneous controlled study included 27 clinically healthy women with uncomplicated pregnancy (control group) and 30 women with symmetric FGR (main group). The study included clinical, clinical laboratory and functional examination methods. The material for the study was placental tissue. The method of differential ultracentrifugation was used to isolate proteins of subcellular fractions of the placenta. Indicators of post-translational modification of proteins (amidation, amination, carbonylation, phosphorylation) were evaluated using spectrophotometric and radioisotope methods.
RESULTS
Women in both groups did not statistically differ in obstetric and somatic anamnesis. In FGR, which developed against the background of placental dysfunction, there are significant changes in placental proteins: the intensity of their cyclonucleotide-dependent phosphorylation, amidation, amination decreases, and spontaneous and metal-catalyzed oxidative carbonylation increases. The degree of these changes depends on the cyclic nucleotide, subcellular localization of proteins, and the characteristics of the studied functional groups. The identified violations are reflected at different levels of protein structure and, consequently, their regulatory properties.
CONCLUSIONS
The revealed violations of the structure of mitochondrial and cytoplasmic proteins of the placenta, which perform numerous regulatory functions, may be important links in the chain of molecular disorders in FGR.
