Assistant ProfessorPhone: (601) 984-2320
Preeclampsia is a pregnancy specific disease that occurs in 5-10% of pregnancies worldwide. The disease is characterized as hypertension after the 20th week of pregnancy associated with new-onset proteinuria, endothelial dysfunction, systemic vasoconstriction, and an increased risk for cardiovascular disease later in life.
A substantial amount of evidence suggests lack of spiral artery remodeling resulting in placental ischemia/hypoxia is the initiating event in the disease process. However, the factors contributing to the reduced vascular remodeling are unknown and a better understanding of placentation and the pathophysiology of the preeclamptic placenta is needed. Therefore, my research focuses around the central hypothesis that increases in CYP4A expression and production of 20-HETE in the placental vasculature leads to the abnormal spiral artery remodeling, reductions in placental perfusion, and triggers placental hypoxia/ischemia. Utilizing unique CYP4A transgenic and knockout rats on the Dahl S genetic background, in addition to a translational element by profiling the metabolism of AA and the expression of CYP4A enzymes in spiral arteries microdissected from the placenta of normal pregnant and preeclamptic women, we plan to test this hypothesis.
Through this research, it is our goal to better understand how these factors are involved in the lack of vessel remodeling during preeclampsia. With this knowledge, new therapies geared toward increasing or decreasing these vessel factors can be developed. These therapies have potential to improve the outcomes of both mother and baby, in addition to the cardiovascular health of the mother later in life.
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