The Impact of Maternal-Fetal Genetic Conflict Situations on the Pathogenesis of Preeclampsia

Preeclampsia leads to maternal and perinatal morbidity and mortality. The literature in English was reviewed to summarize recent advances in understanding the global gene expression changes in the pathogenesis of preeclampsia. We identified at least eight consistently enriched categories, relating to pregnancy maintenance, metabolism, oxidative stress, cell cycle regulation, implantation, decidualization, immune modulation, and vascular function. Expression profiling in preeclampsia placenta and normal placenta revealed 140 transcripts that were significantly differentially expressed, 30 (21.4%) of which were evolved for the protection of the mother, approximately three times less than the number of genes evolved for the benefit of the fetus [110 genes (78.6%)] in preeclampsia placenta versus normal placenta. The genome-wide analysis emphasizes the dysfunctional decidualization as the main mechanism involved in the development of preeclampsia. These genetic signaling events may occur from an imbalance in the maternal-fetal genetic response in the affected placenta. This is to our knowledge the first report on the pathogenesis of preeclampsia, in which preeclampsia may occur as a genetic consequence of maternal-fetal conflict situations during the early decidualization process.