Obstetrics and Gynaecology - Research Publications

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Author: Zhou, Wei × Author: So, Teresa ×

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    Galectin-7: A Novel Placental-released Driver of Preeclampsia.
    Menkhorst, E ; Zhou, W ; So, T ; Santos, L ; Zhang, J-G ; Syngelaki, A ; Nicolaides, K ; St-Pierre, Y ; Dimitriadis, E (SPRINGER HEIDELBERG, 2020-03)
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    Galectin-7 Impairs Placentation and Causes Preeclampsia Features in Mice
    Menkhorst, E ; Zhou, W ; Santos, LL ; Delforce, S ; So, T ; Rainczuk, K ; Loke, H ; Syngelaki, A ; Varshney, S ; Williamson, N ; Pringle, K ; Young, MJ ; Nicolaides, KH ; St-Pierre, Y ; Dimitriadis, E (American Heart Association, 2020-10-01)
    Preeclampsia is a serious pregnancy-induced disorder unique to humans. The etiology of preeclampsia is poorly understood; however, poor placental formation is thought causal. Galectin-7 is produced by trophoblast and is elevated in first-trimester serum of women who subsequently develop preeclampsia. We hypothesized that elevated placental galectin-7 may be causative of preeclampsia. Here, we demonstrated increased galectin-7 production in chorionic villous samples from women who subsequently develop preterm preeclampsia compared with uncomplicated pregnancies. In vitro, galectin-7 impaired human first-trimester trophoblast outgrowth, increased placental production of the antiangiogenic sFlt-1 splice variant, sFlt-1-e15a, and reduced placental production and secretion of ADAM12 (a disintegrin and metalloproteinase12) and angiotensinogen. In vivo, galectin-7 administration (E8–E12) to pregnant mice caused elevated systolic blood pressure, albuminuria, impaired placentation (reduced labyrinth vascular branching, impaired decidual spiral artery remodeling, and a proinflammatory placental state demonstrated by elevated IL1β, IL6 and reduced IL10), and dysregulated expression of renin-angiotensin system components in the placenta, decidua, and kidney, including angiotensinogen, prorenin, and the angiotensin II type 1 receptor. Collectively, this study demonstrates that elevated galectin-7 during placental formation contributes to abnormal placentation and suggests that it leads to the development of preeclampsia via altering placental production of sFlt-1 and renin-angiotensin system components. Targeting galectin-7 may be a new treatment option for preeclampsia.