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Updated: Mar 24, 2026

Author Spotlight: Modeling an Aspect of Preeclampsia in Female Mice Using Hypoxic Human Placenta-Derived Small Extracellular Vesicles
Published on: January 26, 2024
Elevated placental expression at the maternal-fetal interface but diminished maternal circulatory kisspeptin in
Mushi Matjila1, Robert Millar2, Zephne van der Spuy3
1MRC/UCT Receptor Biology Unit, Institute of Infectious Disease and Molecular Medicine, Division of Medical Biochemistry, University of Cape Town, 7925, South Africa; Department of Obstetrics and Gynaecology, Groote Schuur Hospital, Cape Town 7937, South Africa.
Objective:
To 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.
Setting:
Secondary and Tertiary Hospital Setting in Cape Town, South Africa.
Population:
Patients with and without preeclampsia undergoing elective caesarean delivery.
Methods:
The 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 Measures:
Maternal-fetal tissue mRNA expression of Kiss-1 and GPR-54 as well as maternal/cord serum kisspeptin concentrations in healthy and preeclamptic pregnancies.
Results:
There 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.
Conclusions:
Increased 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.
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