The ability of the placenta to exchange nutrients, gasses and wastes between the maternal and fetal circulations is key for adequate fetal growth. Placentae from pregnancies affected by fetal growth restriction exhibit deficiencies in the anatomical structures required for optimal exchange including; 1) the extent of villus branching, 2) the outer syncytiotrophoblast layer of the placenta that transports nutrients into the placenta, and 3) the placental vascular network that transports these nutrients to the fetus. However, our understanding of exactly how these deficiencies impact placental function and why they occur is poor. Mesenchymal stem cells (MSCs) are thought to contribute directly to the initial vasculogenesis events in the placenta in early pregnancy, and reside in a perivascular niche throughout gestation where they are likely play ongoing roles in regulating branching and non-branching angiogenesis. In addition to their normal function within tissues, MSCs have also been used as therapeutic agents in a range of organ systems, where they are effective in dampening inflammation in tissues and promoting wound repair, in part by stimulating angiogenesis. This raises the intriguing possibility that placental MSCs could one day be used as therapeutic agents to treat fetal growth restriction by bolstering placental angiogenesis. In this talk, data will be presented that combines in silico and in vitro approaches to 1) relate published anatomical deficiencies in placental vascularisation in fetal growth restricted pregnancies to placental function, 2) determine how placental MSCs from normal and growth restricted placentae may influence placental angiogenesis by paracrine mechanisms and 3) explore the fate of MSCs transplanted into placental explants in vitro.