Hung, Hsuan-ning

Preeclampsia (PE) incidence in Taiwan is 2-5%, less than the average rate of 5-7% worldwide; however, it is one of the three major causes of maternal death in Taiwan. Unfortunately, the cause of PE remains unclear. PE is associated with abnormal placentation, reduced placental perfusion and systemic vasospasm. It is assumed that PE can be divided into two stages: In the pre-clinical stage, insufficient trophoblast invasion in the first half of pregnancy results in poor placentation. Subsequent uteroplacental insufficiency leads to placental ischemia and oxidative stress. The ischemic and oxidatively stressed placenta releases pro- inflammatory cytokines, lipid peroxidation products and trophoblast debris into the maternal circulation, which in turn trigger an exaggerated maternal systemic inflammatory response as well as cause a variety of symptoms of PE. This study used microarray analysis of differential gene expression in human placentas from PE and normal pregnancies, and then investigate whether the differential gene expression connected with signal transduction of leukocyte transendothelial migration. The results showed that vascular endothelial growth factor 1 (VEGF-1) and cell adhesion molecules 1 (CADM-1) in PE group higher than the normal pregnancies group. The cell adhesion molecule may play a role in the pathophysiology of PE. VEGF-1 and CADM-1 expression are up-reaglated upon stimulation by inflammatory mediators, probably by contributing to the reduced trophoblast invasion and increased vascular damage. These may be useful biomarkers in predicting PE

Differential gene expression in human placentas from preeclampsia and normal pregnancies

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