Preeclampsia, a maternal hypertensive condition, is a new risk factor for cardiovascular disease. Key proteins of interest in the disorder are vascular endothelial growth factor and its endogenous antagonist, soluble Flt-1 (sFlt-1). My research activity has focused on understanding their signaling transduction in endothelial cells and placenta. Previously I identified sFlt-1, which is elevated in pregnancies complicated with preeclampsia, as the principal factor responsible for the reduced placental angiogenesis associated with preeclampsia. Ongoing work is aimed at the development of novel in vivo models for preeclampsia and the use of transgenic animals to define how sFlt-1 causes preeclampsia-like condition. Specifically, I am interested in the interaction of these factors with pro-atherogenic chemokines and their role in the disease progression.

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