Zinc Trafficking in the Placenta
As the interface between maternal tissues and the fetus, placenta plays
an essential role in ensuring optimal pre-natal development. 
The placenta is comprised of numerous cell types including placental trophoblasts which
exhibit functional temporality. During early pregnancy, proliferative cytotrophoblasts are
responsible for invasion and implantation of the blastocyst into the uterine endothelium,
after which these cells differentiate into multinucleated syncitiotrophoblasts that function
to transport nutrients to the developing fetus. A relationship between maternal nutrition
and poor cytotrophoblast invasivity has long been recognized and adverse outcomes including
pre-elcampsia, spontaneous abortion and maternal infertility highlight the importance of
placental nutrient transport. The dependence upon optimal zinc transfer for fetal development
necessitates the coordinated regulation of zinc transfer from maternal circulation across the
trophoblast to the developing fetus. Our laboratory explores the regulation of zinc transport
by nutritional, environmental and hormonal factors in placental trophoblasts and aims to
delineate unique roles for specific zinc transporters within this specialized cell-type.
Fetal growth restriction, pre-eclampsia and pre-term birth
Infants born with low birth weight account for ~10-15% of all pregnancies and low birth weight is predominantly caused by fetal growth restriction, pre-eclampsia and pre-term birth. These infants die at rates >40 times those of normal weight infants and are at much greater risk for the development of major diseases later in life such as coronary heart disease, hypertension and diabetes. The reproductive hormone progesterone is considered to be the primary determinant of female fertility, and studies have suggested that progesterone administration may reduce the incidence of these disorders, illustrating the importance of this hormone in optimizing fetal growth and development. Progesterone regulates numerous processes via genotrophic mechanisms through the activation of progesterone receptors which subsequently bind to progesterone response elements in the promoters of many genes. We have recently uncovered novel, non-genomic progesterone-activated effects on zinc trafficking in trophoblasts. Our laboratory explores the intracellular signaling mechanisms and the functional consequences of progesterone-activated zinc trafficking in this unique cell-type to provide a better understanding of the role that maternal exposure to nutritional, environmental and hormonal factors play on placentation and micronutrient transport to the fetus affecting infant health and disease.