Placental mRNA Expression of Neurokinin B Is Increased in PCOS Pregnancies with Female Offspring

Current research suggests that polycystic ovary syndrome (PCOS) might originate in utero and implicates the placenta in its pathogenesis. Kisspeptin (KISS1) and neurokinin B (NKB) are produced by the placenta in high amounts, and they have been implicated in several pregnancy complications associated with placental dysfunction. However, their placental expression has not been studied in PCOS. We isolated mRNA after delivery from the placentae of 31 PCOS and 37 control women with term, uncomplicated, singleton pregnancies. The expression of KISS1, NKB, and neurokinin receptors 1, 2, and 3 was analyzed with real-time polymerase chain reaction, using β-actin as the reference gene. Maternal serum and umbilical cord levels of total testosterone, sex hormone-binding globulin (SHBG), free androgen index (FAI), androstenedione, dehydroepiandrosterone sulfate (DHEAS), Anti-Mullerian hormone (AMH), and estradiol were also assessed. <i>NKB</i> placental mRNA expression was higher in PCOS women versus controls in pregnancies with female offspring. <i>NKB</i> expression depended on fetal gender, being higher in pregnancies with male fetuses, regardless of PCOS. <i>NKB</i> was positively correlated with umbilical cord FAI and AMH, and <i>KISS1</i> was positively correlated with cord testosterone and FAI; there was also a strong positive correlation between <i>NKB</i> and <i>KISS1</i> expression. Women with PCOS had higher serum AMH and FAI and lower SHBG than controls. Our findings indicate that NKB might be involved in the PCOS-related placental dysfunction and warrant further investigation. Studies assessing the placental expression of <i>NKB</i> should take fetal gender into consideration.