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Phosphoglucomutase 5 gene transcripts are expressed by the human placenta and differentially regulated in placental dysfunction
Phosphoglucomutase 5 gene transcripts are expressed by the human placenta and differentially regulated in placental dysfunction
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Phosphoglucomutase 5 gene transcripts are expressed by the human placenta and differentially regulated in placental dysfunction
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Phosphoglucomutase 5 gene transcripts are expressed by the human placenta and differentially regulated in placental dysfunction
Phosphoglucomutase 5 gene transcripts are expressed by the human placenta and differentially regulated in placental dysfunction

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Phosphoglucomutase 5 gene transcripts are expressed by the human placenta and differentially regulated in placental dysfunction
Phosphoglucomutase 5 gene transcripts are expressed by the human placenta and differentially regulated in placental dysfunction
Journal Article

Phosphoglucomutase 5 gene transcripts are expressed by the human placenta and differentially regulated in placental dysfunction

2025
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Overview
The placenta plays an essential role facilitating nutrient, gas and waste exchange between the maternal and fetal systems for optimal fetal growth. When placental development is impaired and the placenta dysfunctional, serious pregnancy complications such as fetal growth restriction and preeclampsia may arise. Previously, phosphoglucomutase-5 (PGM5) transcripts were found to be highly elevated in the blood of patients whose pregnancies were complicated by fetal growth restriction and preeclampsia. As both conditions feature placental insufficiency, here we aimed to characterise PGM5 levels in the healthy and dysfunctional placenta. PGM5 expression was detectable in all placental samples across gestation, in cases of preterm preeclampsia, fetal growth restriction and controls. PGM5 mRNA expression was significantly downregulated in the pathological placentas compared to controls, but PGM5 protein production was not dysregulated. Isolated cytotrophoblast and placental explant tissue exposed to hypoxia (modelling placental dysfunction) demonstrated significantly increased PGM5 expression, but again did not change protein levels. Silencing PGM5 expression under hypoxic conditions in primary cytotrophoblast did not alter anti-angiogenic sFLT-1 secretion but increased expression of multiple genes associated with cell growth, apoptosis and oxidative stress, whilst also increasing cell viability. Expression of PGM5 in all placental samples assessed suggests that PGM5 has functions in the placenta. However, further investigation could be performed to explore the discrepancies in protein and mRNA expression, as well as the precise function of PGM5 in the placenta, and whether altered PGM5 levels may be important for placental development.