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Placental invasion of maternal decidua is a complex and incompletely characterized process. When invasion is insufficient, as in the case of preeclampsia, both the mother and fetus can experience harm. The current model of preeclampsia is that the placenta fails to develop properly early in gestation, which leads to toxic factor secretion into the maternal system in late gestation. The latter events lead to the clinical signs of preeclampsia, including hypertension, edema and proteinuria. Toward understanding placental development, micorarray studies in the Winn lab have identified genes involved in the development of normal and preeclamptic placentas across gestation. In these studies it was found that Siglec-6 is upregulated in preeclamptic placentas near term when compared to age matched controls. Siglec-6 is a transmembrane receptor expressed in placental and B-cells whose biology is not well characterized. Siglec-6 was originally cloned as a leptin binding partner. Leptin is well known in the regulation of energy homeostasis, but overexpression has also been demonstrated in preeclampsia. I am investigating the roles of Siglec-6 and Leptin in placental development and in the pathogenesis of preeclampsia.