Placental glycocode signalling networks in preeclampsia: Implication for maternal and fetal health

Abstract

The proper development of the placenta, a temporary organ formed during pregnancy, is of great importance for fetal survival and pregnancy progress. The complex interaction between maternal cells and highly-glycosylated fetal trophoblasts contributes to the function of this important organ. Disruption of this maternal-fetal molecular dialogue leads to placental abnormalities and subsequent preeclampsia (PE), a life-threatening pregnancy disorder with long-term adverse effects on the health of both mother and offspring. Galectin-1 (gal-1), a glycan-binding protein abundantly expressed at the feto-maternal interface, serves as a predominant decipherer of glycocode involved in multiple key reproductive processes, while its down-regulation or deficiency is associated with PE development. However, the impact of maternal- and fetoplacental-derived gal-1 on the pathogenesis of PE is not well understood. The present study demonstrated that deficiency of gal-1 in the maternal niche during pregnancy induced PE-like syndrome and cardiovascular maladaptation in mice, which is accompanied by aberrant placental development and function during pre- and post-placentation periods. Mechanistically, maternal-derived gal-1 dominates the invasive capacity of trophoblast cells through differential placental Sda-terminal N glycosylation. Thus, the current findings highlight the unique contribution of maternal-derived gal-1 to placental development and the involvement of compromised gal-1 signaling pathway within the maternal compartment in the pathogenesis of PE.