Abstract
Despite the differences in the clinical manifestations of major obstetric syndromes, such as preeclampsia (PE) and intrauterine growth restriction (IUGR), their pathogenesis is based on the dysregulation of proliferation, differentiation, and invasion of cytotrophoblast cells that occur in the developing placenta, decidual endometrium, and myometrial parts of the spiral arteries. To understand the similarities and differences in the molecular mechanisms of PE and IUGR, samples of the placental bed and placental tissue were analyzed using protein mass spectrometry and the deep sequencing of small RNAs, followed by validation of the data obtained by quantitative RT-PCR in real time. A comparison of the transcriptome and proteomic profiles in the samples made it possible to conclude that the main changes in the molecular profile in IUGR occur in the placental bed, in contrast to PE, in which the majority of molecular changes occurs in the placenta. In placental bed samples, significant changes in the ratio of miRNA and its potential target gene expression levels were revealed, which were unique for IUGR (miR-30c-5p/VIM, miR-28-3p/VIM, miR-1-3p/ANXA2, miR-30c-5p/FBN1; miR-15b-5p/MYL6), unique for PE (miR-185-3p/FLNA), common for IUGR and PE (miR-30c-5p/YWHAZ and miR-654-3p/FGA), but all associated with abnormality in the hemostatic and vascular systems as well as with an inflammatory process at the fetal‒maternal interface.
Highlights
Abnormal placentation due to multiple causes is considered a key pathogenetic mechanism of various pregnancy complications, preeclampsia (PE) and intrauterine growth restriction (IUGR) [1]
There were no differences between patient groups in terms of maternal age, body mass index (BMI), pulsatility index (PI) of middle cerebral artery (MCA), or PI of left uterine artery
There were significant differences between patient groups with complicated pregnancies and the control group in terms of blood pressure, APGAR 1 min and 5 min, indicator of fetal condition according to cardiotocography (CTG) data, PI of right uterine artery, birth weight, placental weight, PI of umbilical artery, percentile of estimated fetal weight, gestational age at the time of delivery, and cerebroplacental ratio
Summary
Abnormal placentation due to multiple causes is considered a key pathogenetic mechanism of various pregnancy complications, preeclampsia (PE) and intrauterine growth restriction (IUGR) [1]. The lateonset type of PE, with clinical manifestation after 34 gestation weeks (GW), comprises more than 80% of all PE cases and is associated with normal or only slightly altered behavior of the uterine spiral arteries and no signs of fetal growth restriction. The early-onset type of PE (clinical manifestation before 34 GW) comprises the most severe cases of PE (5–20%) and is associated with incomplete trophoblast invasion of maternal spiral arteries, resulting in changes in the blood flow in the uterine arteries, placental vessels, and umbilical arteries, with signs of fetal growth restriction. IUGR is a condition that affects 5–10% of pregnancies, characterized by slow intrauterine growth of the fetus with an expected fetal weight below the 10th percentile, assessed for gestational age and gender, associated with abnormal Doppler ultrasound findings in the vessels of fetus and umbilical cord [7,8]. IUGR (diagnosed at or below 32 GW) differs from late-onset IUGR (diagnosed after 32 GW) in terms of its clinical manifestations, association with hypertension, patterns of deterioration, and severity of placental dysfunction [9]
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