What is it about?

This study discovered that differentiation of trophoblasts toward syncytium triggers an endocytosis strategy, macropinocytosis, to uptake large extracellular molecules. This unique machinery of nutrient uptake is strikingly boosted via inhibition of mTOR under amino acid shortage conditions, which is essential for fetal survival.

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Why is it important?

The findings underscore a novel and physiologically important compensatory pathway for placental multinucleated trophoblasts to achieve a prime goal of nutrient delivery in the context of poor blood flow or other limitations in maternal nutrient supply. The study may facilitate the development of potential treatments to support fetus that suffers from maternal malnutrition or other conditions leading to insufficient nutritional transport.

Perspectives

During pregnancy, maternal-fetal material exchange predominantly depends on the placenta. Lining at the outer surface of the placental villi, the syncytiotrophoblast (STB) is directly bathed in maternal blood, and thus positioned to take charge of maternal-fetal exchanges of gases, nutrients, and waste. STB has been identified as the largest multinucleated epithelial surface in the body, yet the advantages of such an extensively multinucleated cellular structure in substance exchange remains poorly understood. This study discovered that differentiation of trophoblasts toward syncytium triggers an endocytosis strategy, macropinocytosis, to uptake large extracellular molecules. This unique machinery of nutrient uptake is strikingly boosted via inhibition of mTOR under amino acid shortage conditions, which is essential for fetal survival.

Xuan Shao
Institute of Zoology, Chinese Academy of Sciences

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This page is a summary of: Placental trophoblast syncytialization potentiates macropinocytosis via mTOR signaling to adapt to reduced amino acid supply, Proceedings of the National Academy of Sciences, January 2021, Proceedings of the National Academy of Sciences, DOI: 10.1073/pnas.2017092118.
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