Elevated placental expression at the maternal-fetal interface but diminished maternal circulatory kisspeptin in preeclamptic pregnancies

- Placental bed kisspeptin expression is low in healthy and preeclamptic pregnancies.
- Placental kisspeptin is elevated but serum levels diminished in preeclampsia.
- Circulatory kisspeptin has potential as a marker of placental dysfunction.

ObjectiveTo investigate the placental mRNA and protein expression of metastasis suppressor gene Kiss-1 and the transcript expression of its receptor GPR-54 across the maternal-fetal interface of healthy and preeclamptic pregnancies. To furthermore compare placental tissue kisspeptin expression to circulatory kisspeptin levels in these pregnancies.SettingSecondary and Tertiary Hospital Setting in Cape Town, South Africa.PopulationPatients with and without preeclampsia undergoing elective caesarean delivery.MethodsThe placenta, placental bed and decidua parietalis as well as maternal and cord blood in both healthy and preeclamptic pregnancies were simultaneously sampled at elective caesarean delivery. RT-PCR was utilised to determine mRNA expression while immunohistochemistry was employed to investigate protein expression in maternal-fetal tissues. Circulating maternal and cord serum kisspeptin concentrations were determined using ELISA.Main outcome measuresMaternal-fetal tissue mRNA expression of Kiss-1 and GPR-54 as well as maternal/cord serum kisspeptin concentrations in healthy and preeclamptic pregnancies.ResultsThere was high placental kisspeptin expression but low circulating serum kisspeptin levels in pregnancies complicated by preeclampsia. Kiss-1 mRNA and protein expression was minimal in the maternal tissues (placental bed and decidua parietalis) of both healthy and preeclamptic pregnancies. No difference was found in Kiss-1 receptor (GPR-54) mRNA expression across maternal-fetal tissues of healthy and preeclamptic pregnancies.ConclusionsIncreased placental kisspeptin expression is consistent with reduced trophoblast invasiveness and may represent a molecular mechanism that explains the development of preeclampsia. Decreased circulating kisspeptin concentration has the potential to be utilised as a marker for placental dysfunction.