P–597 Placental expression of neurokinin B and its receptor NK3R is increased in women with polycystic ovary syndrome: results of a preliminary study
Authors: Markantes G , Markatos F , Georgopoulos N 
Published: August 2021

Abstract

Study question
Is the placental expression of neurokinin B (NKB) and its receptors NK1R, NK2R and NK3R affected by the polycystic ovary syndrome (PCOS)? Summary answer: The placental expression of NKB and NK3R is increased in PCOS, while the expression of NK1R and NK2R is not affected. What is known already: Women with PCOS are at increased risk of pregnancy complications and poor pregnancy outcomes. Defective placentation is among the proposed mechanisms involved. Altered NKB placental expression has been associated with several conditions characterized by placental dysfunction, such as pre-eclampsia and intra-uterine growth retardation. To our knowledge, the expression of NKB and its receptors has not been studied in placental tissue of women with PCOS.

Study design, size, duration
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.

Participants/materials, setting, methods
At delivery, placental specimens were collected and immediately submerged in RNAlater solution. Samples were stored at –20oC 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).

Main results and the role of chance
The placental mRNA expression of NKB and NK3R was significantly higher in PCOS women versus controls (2.4-fold, p &lt; 0.05 for NKB and 7-fold, p &lt; 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.

Limitations, reasons for caution
The main limitation of this study is the small sample size. Expanding the number of participants is the necessary next step, in order to corroborate our preliminary findings. Furthermore, correlations between the placental expression of NKB, NK1R, NK2R, NK3R and maternal sex steroids, glucose and insulin levels should be sought.
Wider implications of the findings: 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.

Trial registration number
Not applicable