Pre-eclampsia (PE) is a serious disease of pregnancy affecting 4 million women/year. The disease etiology is complex but its origin lies in abnormal placental development and function. PE is associated with increased nitrative stress and abnormal renewal of syncytiotrophoblast (STB), the transport epithelium of human placenta. STB is renewed by cytotrophoblast cells (CTB) that proliferate, differentiate, and fuse with the multinucleated STB and this is balanced by apoptosis and shedding of aged nuclei. In non-placental tissues the amino acid taurine regulates proliferation, differentiation, and apoptosis. Taurine is accumulated in STB by the taurine transporter (TauT) and we have shown that TauT activity is significantly lower in PE compared to normal pregnancy1. TauT activity can be downregulated by nitrative stress and in PE those placentas with a lower TauT activity also had elevated nitrotyrosine expression, a marker of nitrative stress. Furthermore, generation of STB nitrative stress in vitro with SIN-1 reduced TauT activity by 14%2. Here we test the hypothesis that reducing placental TauT activity by nitrative stress alters CTB proliferation and apoptosis. Placental villous explants from normal pregnancy were cultured for 7 days. On day 5 explants were treated with 1mM SIN-1 for 48hrs to reduce TauT activity. Immunohistochemistry was used to assess proliferation (detected by Ki67) and apoptosis (detected by M30: caspase-cleaved cytokeratin). The apoptotic index was calculated as the area of M30-positive staining expressed as a percent of total villous area using image pro plus software. To quantify proliferation explants were dual stained for ki67 and the CTB marker E-cadherin. Proliferation index was calculated as the number of cells positive for both ki67 and E-cadherin (i.e. proliferating CTB) expressed as a percent of the total number of E-cadherin positive cells (i.e. CTB). For each experiment, 8 fields of view were assessed and a mean calculated. There was no difference in villous area or number of CTB between control and SIN-1 treated placental explants. SIN-1 treatment significantly reduced CTB proliferative index (Fig1) and significantly increased apoptotic index compared to controls (Fig2). Inspection of stained tissue sections showed morphological integrity was maintained throughout culture and secretion of hCG, an indicator of endocrine viability, was unaffected by SIN-1 treatment. Nitrative stress reduces placental TauT activity2, inhibits CTB proliferation and increases apoptosis. Future work will determine whether this abnormal STB renewal is a direct effect of nitrative stress or a result of reduced TauT activity. We propose that in PE placental TauT activity is reduced by nitration, leading to altered CTB proliferation and apoptosis, resulting in abnormal renewal of the STB.