Human umbilical cord mesenchymal stem cells (hUMSCs) could provide a valuable tool for the 'rehabilitation' of dysfunctional trophoblast cells, allowing them to perform their essential roles for the development of the placenta through paracrine properties. In fact, an increased oxidative stress, which can be observed in pregnancies complicated by PE or IUGR, has been reported to be accompanied by an augmented iNOS expression and higher release of NO, which is converted to harmful peroxynitrite after reaction with superoxide.

It is important to underline the fact that an excess of NO can have deleterious rather than protective effects. An increase in systemic and uteroplacental NO, due to an overexpression of the inducible isoform of NOS and an uncoupling of the endothelial NOS (eNOS), have been widely documented in animal models of PE. The balance of NO release by various NO synthases (NOS) could be at the basis of the onset of preeclamptic disorders. Nitric oxide (NO) can also play a fundamental role, being involved in blood flow regulation in the placental fetal vascular bed. The subsequent peroxidation causes endothelial damage and changes in the release of pro-angiogenetic/vasodilating factors, which potentiate the endothelial dysfunction.

During placentation, failure in remodeling of the spiral arteries by trophoblasts contributes to the development of pregnancy-related pathologies, such as preeclampsia (PE) and intrauterine growth restriction (IUGR) via the excessive formation of reactive oxygen species (ROS).

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