Supplemental Digital Content is available in the text. 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.

中文翻译：

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Galectin-7 损害胎盘并导致小鼠先兆子痫特征

补充数字内容在文本中可用。先兆子痫是一种严重的妊娠引起的人类特有的疾病。先兆子痫的病因知之甚少。然而，胎盘形成不良被认为是因果关系。Galectin-7 由滋养层细胞产生，在随后发展为先兆子痫的妇女的妊娠早期血清中升高。我们假设胎盘半乳糖凝集素 7 升高可能是先兆子痫的原因。在这里，我们证明了与无并发症妊娠相比，随后发生早产先兆子痫的女性的绒毛膜绒毛样本中的半乳糖凝集素 7 产量增加。在体外，半乳糖凝集素 7 损害了人类妊娠早期滋养细胞的生长，增加了抗血管生成 sFlt-1 剪接变体 sFlt-1-e15a 的胎盘产生，ADAM12（一种去整合素和金属蛋白酶12）和血管紧张素原的胎盘产生和分泌减少。在体内，对怀孕小鼠给予半乳糖凝集素 7 (E8-E12) 导致收缩压升高、蛋白尿、胎盘受损（迷路血管分支减少、蜕膜螺旋动脉重塑受损，以及由升高的 IL1β、IL6 和降低证明的促炎胎盘状态） IL10)，以及胎盘、蜕膜和肾脏中肾素-血管紧张素系统成分的表达失调，包括血管紧张素原、肾素原和血管紧张素 II 1 型受体。总的来说，该研究表明，胎盘形成过程中半乳糖凝集素 7 升高会导致胎盘异常，并表明它通过改变胎盘 sFlt-1 和肾素-血管紧张素系统成分的产生而导致先兆子痫的发展。靶向半乳糖凝集素 7 可能是先兆子痫的新治疗选择。