The differential expression of Kiss1, MMP9 and angiogenic regulators across the feto-maternal interface of healthy human pregnancies: implications for trophoblast invasion and vessel development.
Matjila. Mushi M; Millar. Robert R; van der Spuy. Zephne Z; Katz. Arieh A
Key Findings
- Kiss1 and its receptor Kiss1R are expressed at higher levels in the placenta than in the maternal decidua or placental bed.
- VEGF‑A is most abundant in the maternal placental bed, while VEGFR2 (its main receptor) is also highest there, indicating a maternal‑driven angiogenesis pathway.
- The PROK1/PROK1R system is most active in the placenta, suggesting a separate fetal‑specific angiogenesis pathway.
Practical Outcomes
- For biohackers, there are no direct applications: the findings are specific to pregnancy biology and do not translate into dosage recommendations, performance boosts, or longevity strategies. The study mainly adds basic science knowledge about how kisspeptin works in fetal‑maternal communication.
Summary
This study looked at where the kisspeptin gene (Kiss1) and related proteins are turned on in the placenta and surrounding maternal tissues during a healthy pregnancy. It found that kisspeptin and its receptor are most active in the fetal side of the placenta, while different blood‑vessel growth signals dominate on the maternal side. The work helps scientists understand how the baby and mother coordinate blood‑vessel formation, but it doesn’t give any tips you can use for health, performance, or longevity outside of pregnancy.
Abstract
Genes involved in invasion of trophoblast cells and angiogenesis are crucial in determining pregnancy outcome. We therefore studied expression profiles of these genes in both fetal and maternal tissues to enhance our understanding of feto-maternal dialogue. We investigated the expression of genes involved in trophoblast invasion, namely Kiss1, Kiss1 Receptor (Kiss1R) and MMP9 as well as the expression of angiogenic ligands Vascular Endothelial Growth Factor-A (VEGF-A) and Prokineticin-1 (PROK1) and their respective receptors (VEGFR1, VEGFR2 and PROK1R) across the feto-maternal interface of healthy human pregnancies. The placenta, placental bed and decidua parietalis were sampled at elective caesarean delivery. Real-time RT-PCR was used to investigate transcription, while immunohistochemistry and western blot analyses were utilized to study protein expression. We found that the expression of Kiss1 (p<0.001), Kiss1R (p<0.05) and MMP9 (p<0.01) were higher in the placenta compared to the placental bed and decidua parietalis. In contrast, the expression of VEGF-A was highest in the placental bed (p<0.001). While VEGFR1 expression was highest in the placenta (p<0.01), the expression of VEGFR2 was highest in the placental bed (p<0.001). Lastly, both PROK1 (p<0.001) and its receptor PROK1R (p<0.001) had highest expression in the placenta. Genes associated with trophoblast invasion were highly expressed in the placenta which could suggest that the influence on invasion capacity may largely be exercised at the fetal level. Furthermore, our findings on angiogenic gene expression profiles suggest that angiogenesis may be regulated by two distinct pathways with the PROK1/PROK1R system specifically mediating angiogenesis in the fetus and VEGFA/VEGFR2 ligand-receptor pair predominantly mediating maternal angiogenesis.
Study Information
pubmed
2013
2013-05-16T00:00:00.000Z
10.1371/journal.pone.0063574
32
52