Study summary · research use only
The AKT1-FOXO4 axis reciprocally regulates hemochorial placentation
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
In this rat study using a genome-edited/loss-of-function model, the authors investigated roles of AKT1 and Forkhead box O4 (FOXO4) in hemochorial placentation. Disruption of AKT1 resulted in placental, fetal, and postnatal growth restriction. Foxo4, abundantly expressed in the junctional zone and invasive trophoblast cells, was disrupted by genome editing, resulting in placentomegaly including an enlarged junctional zone. AKT1 and FOXO4 regulated expression of many of the same trophoblast transcripts, but in opposite directions. The authors describe AKT1 and FOXO4 as part of a regulatory network that reciprocally controls indices of placenta development.
Abstract
Hemochorial placentation involves the differentiation of invasive trophoblast cells, specialized cells that possess the capacity to exit the placenta and invade into the uterus where they restructure the vasculature. Invasive trophoblast cells arise from a well-defined compartment within the placenta, referred to as the junctional zone in rat and the extravillous trophoblast cell column in human. In this study, we investigated roles for AKT1, a serine/threonine kinase, in placental development using a genome-edited/loss-of-function rat model. Disruption of AKT1 resulted in placental, fetal and postnatal growth restriction. Forkhead box O4 (Foxo4), which encodes a transcription factor and known AKT substrate, was abundantly expressed in the junctional zone and in invasive trophoblast cells of the rat placentation site. Foxo4 gene disruption using genome editing resulted in placentomegaly, including an enlarged junctional zone. AKT1 and FOXO4 regulate the expression of many of the same transcripts expressed by trophoblast cells, but in opposite directions. In summary, we have identified AKT1 and FOXO4 as part of a regulatory network that reciprocally controls critical indices of hemochorial placenta development.
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