Placental GDF15 supports fetal growth in mouse experiments
Removing a placental protein restricted fetal growth in mice, while an experimental delivery approach improved growth measures in an animal model. A single peer-reviewed study traced GDF15 to a liver signalling pathway and also examined piglets and cells. The work identifies an animal mechanism, with its relevance to human pregnancy still uncertain.
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Placental protein loss restricts growth
Removing Gdf15 specifically from the placenta reduced fetal weight and length in mice. The single peer-reviewed study examined GDF15, a protein made by the placenta, the organ supporting exchange between mother and fetus. Researchers used genetically altered mice, growth-restriction models induced by protein restriction or dexamethasone, piglets and cell experiments. Lower placental and fetal circulating GDF15 accompanied growth restriction in mice and piglets.[1]
The protein reaches a liver growth pathway
Tracking experiments indicated that placental GDF15 entered fetal circulation and accumulated in the liver. Researchers linked it to STAT3, a cellular signalling pathway, and production of IGF2, a growth factor. Blocking STAT3 in fetal liver cells removed the increase in IGF2 induced by GDF15. Reciprocal crosses examined the contribution of maternal GDF15. Its absence had no statistically significant effect on fetal weight or the protein level in fetal circulation.[1]
Targeted delivery improves mouse growth measures
In mice modelling restricted growth, fetal length, weight and related measures improved after delivery of Gdf15 messenger RNA in lipid particles directed to the placenta. Safety and effectiveness in human pregnancy remain untested. How GDF15 crosses from placenta to fetus is still incompletely understood, and the researchers call for prospective human work examining maternal and fetal genetics alongside growth measurements.[1]
