Endocrine Abstracts

Background

Women with polycystic ovary syndrome (PCOS) are at increased risk of pregnancy complications and poor pregnancy outcomes. Defective placentation is among the proposed mechanisms involved. Altered neurokinin B (NKB) placental expression has been associated with several conditions characterized by placental dysfunction, such as pre-eclampsia and intra-uterine growth retardation. However, the expression of NKB and its receptors has not been studied in placental tissue of women with PCOS.

Objective

To compare the placental mRNA expression of NKB and its receptors NK1R, NK2R and NK3R in women with PCOS and controls.

Methods

This was a single-center, prospective, case-control study. Women with PCOS according to the Rotterdam criteria (cases) and healthy pregnant women (controls) were enrolled at first prenatal visit and followed until delivery. Only women with spontaneous conception and singleton, uncomplicated, term pregnancies (10 PCOS and 10 controls) were included in the final analysis. All participants provided informed consent. At delivery, placental specimens were collected and immediately submerged in RNAlater solution. Samples were stored at -20^oC until analysis. The mRNA expression of NKB, NK1R, NK2R and NK3R was quantified by real-time PCR (RT-PCR). The relative mRNA expression was estimated by the ΔΔCT method, using β-actin as reference (housekeeping gene). Statistical analysis was performed using SPSS 25.0, and the level of statistical significance was set at 0.05 (two-sided).

Results

The placental mRNA expression of NKB and NK3R was significantly higher in PCOS women vs controls (2.4-fold, P < 0.05 for NKB and 7-fold, P < 0.05 for NK3R). No significant alterations were observed in the mRNA expression of NK1R and NK2R between the two groups. There was no statistically significant difference regarding age, BMI, caesarian section frequency, offspring sex and birth weight between women with PCOS and controls. The placental expression of NKB and its receptors was correlated neither with maternal age and BMI, nor with offspring birth weight.

Conclusions

The present study is the first to demonstrate increased placental expression of NKB and its receptor NK3R in women with PCOS. These findings support a potential role for NKB as a mediator of placental alterations characterizing PCOS. Expanding the number of participants is the necessary next step, in order to corroborate these preliminary findings. Furthermore, correlations between the placental expression of NKB, NK1R, NK2R, NK3R and PCOS phenotype, maternal sex steroids, glucose and insulin levels should be sought.

Keywords: polycystic ovary syndrome (PCOS), placenta, neurokinin B (NKB), NK3R.