Role of kisspeptin in decidualization and unexplained recurrent spontaneous abortion via the ERK1/2 signalling pathway.

INTRODUCTION

This study aimed to study the expression and function of kisspeptin during human uterine decidualization in recurrent spontaneous abortion (RSA) and the underlying mechanism.

METHODS

All patients were recruited from the Clinical Reproductive Center of the Second Affiliated Hospital of Soochow University. Mice models of RSA (CBA/J × DBA/2) and normal pregnancy (CBA/J × BALB/c) were established, respectively. Kisspeptin expression in the serum and decidual tissues of women with RSA were detected. The function of kisspeptin during decidualization in human endometrial stromal cells (HESCs) was assessed by enhancing and silencing kisspeptin expression. CBA/J × DBA/2 pregnant mice were injected with kisspeptin polypeptide, kisspeptin receptor blocker, and expression of decidualization markers was observed. The regulation of ERK1/2 signalling pathway were verified.

RESULTS

Serum kisspeptin levels were significantly lower in patients with RSA than in normal pregnant individuals, as was the expression of kisspeptin, p-ERK, and decidualization indicators in the decidua. Additionally, kisspeptin inhibition downregulated the expression of decidualization markers in HESCs. In mice with RSA, kisspeptin was significantly downregulated, and p-ERK expression at the maternal-foetal interface was significantly decreased. Moreover, exogenous kisspeptin supplementation improved the levels of IGFBP-1 and dPRL, upregulated p-ERK expression, and reduced the abortion rate.

DISCUSSION: Kisspeptin is involved in promoting uterine decidualization via the ERK1/2 signalling pathway.