Abstract
Taurine is conditionally essential in human pregnancy as fetal tissues do not express the biosynthetic enzyme. Taurine demand by both fetus and placenta must be met by sufficient uptake from maternal blood into syncytiotrophoblast (STB), the transport epithelium of the placenta, via the taurine transporter (TauT). STB TauT activity is reduced in the pregnancy complication pre-eclampsia (PE). This condition is associated with fetal growth restriction (FGR) and placental pathology comprising abnormal STB renewal, mitochondrial dysfunction, and elevated oxidative stress. In non-placental cells intracellular taurine is cytoprotective and regulates proliferation, differentiation, and apoptosis; key events in STB renewal. Here we test the hypothesis that STB taurine deficiency impairs renewal and increases susceptibility to oxidative stress by compromising mitochondrial function.
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