Kandel Manju, Tong Stephen, Walker Susan P, Cannon Ping, Nguyen Tuong-Vi, MacDonald Teresa M, Hannan Natalie J, Kaitu'u-Lino Tu'uhevaha J, Bartho Lucy A
Translational Obstetrics Group, The Department of Obstetrics and Gynaecology, Mercy Hospital for Women, University of Melbourne, Heidelberg, VIC, Australia.
Mercy Perinatal, Mercy Hospital for Women, Heidelberg, VIC, Australia.
Front Physiol. 2022 Oct 14;13:1037597. doi: 10.3389/fphys.2022.1037597. eCollection 2022.
Preeclampsia is a disease of pregnancy responsible for significant maternal and neonatal mortality. Galectin-3 is a -Galactoside binding protein. This study aimed to characterise galectin-3 in women with preeclampsia and human trophoblast stem cells (hTSCs). Galectin-3 was measured in placental lysates and plasma collected from patients with early-onset preeclampsia (delivered <34 weeks' gestation) and gestation matched controls. Placental galectin-3 protein was significantly reduced in 43 women with early-onset preeclampsia compared to 21 controls. mRNA expression of (galectin-3 encoding gene) was reduced in 29 women with early-onset preeclampsia, compared to 18 controls ( = 0.009). There was no significant difference in plasma galectin-3 protein in 46 women with early-onset preeclampsia compared to 20 controls. In a separate cohort of samples collected at 36 weeks' gestation, circulating galectin-3 was not altered in 23 women who later developed preeclampsia, versus 182 who did not. In syncytialised hTSCs, hypoxia increased mRNA expression of ( = 0.01). Treatment with inflammatory cytokines (TNF-α and IL-6) had no effect on mRNA expression However, TNF-α treatment caused an increase in mRNA expression of (galectin-3 binding protein encoding gene) in hTSCs ( = 0.03). This study showed a reduction of galectin-3 in placenta from pregnancies complicated by early-onset preeclampsia. mRNA expression was dysregulated by hypoxia exposure in placental stem cells.
子痫前期是一种妊娠期疾病,可导致严重的孕产妇和新生儿死亡。半乳糖凝集素-3是一种β-半乳糖苷结合蛋白。本研究旨在表征子痫前期患者和人滋养层干细胞(hTSCs)中的半乳糖凝集素-3。在早发型子痫前期患者(妊娠<34周分娩)和妊娠匹配的对照组收集的胎盘裂解物和血浆中测量半乳糖凝集素-3。与21名对照组相比,43名早发型子痫前期患者的胎盘半乳糖凝集素-3蛋白显著降低。与18名对照组相比,29名早发型子痫前期患者中LGALS3(半乳糖凝集素-3编码基因)的mRNA表达降低(P = 0.009)。与20名对照组相比,46名早发型子痫前期患者的血浆半乳糖凝集素-3蛋白无显著差异。在另一组妊娠36周时收集的样本中,23名后来发生子痫前期的女性与182名未发生子痫前期的女性相比,循环半乳糖凝集素-3没有改变。在合体化的hTSCs中,缺氧增加了LGALS3的mRNA表达(P = 0.01)。用炎性细胞因子(TNF-α和IL-6)处理对LGALS3 mRNA表达没有影响。然而,TNF-α处理导致hTSCs中LGALS9(半乳糖凝集素-3结合蛋白编码基因)的mRNA表达增加(P = 0.03)。本研究表明,早发型子痫前期合并妊娠的胎盘组织中半乳糖凝集素-3减少。胎盘干细胞暴露于缺氧环境会导致LGALS3 mRNA表达失调。