合胞滋养细胞
胎盘
内科学
胎儿
内分泌学
脐带
男科
怀孕
生物
脐带血
子痫前期
缺氧(环境)
生物标志物
医学
化学
免疫学
生物化学
遗传学
有机化学
氧气
作者
Ruofan Yao,Penghua Yang,Katherine Goetzinger,Kristin Atkins,Wei-Bin Shen,Bingbing Wang,Peixin Yang
标识
DOI:10.1016/j.reprotox.2022.06.009
摘要
Maternal obesity is associated with an increased risk of adverse pregnancy outcomes including stillbirth, and their etiology is thought to be related to placental and fetal hypoxia. In this study, we sought to investigate the levels of lactate in maternal and umbilical cord blood, a well characterized biomarker for hypoxia, and expression of plasma membrane lactate transporter MCT1 and MCT4 in the placental syncytiotrophoblast (STB), which are responsible for lactate uptake and extrusion, respectively, from pregnant women with a diagnosis of obesity following a Cesarean delivery at term. With use of approaches including immunofluorescence staining, Western blot, RT-qPCR and ELISA, our results revealed that in controls the expression of MCT1 was equally observed between basal (fetal-facing, BM) and microvillous (maternal-facing, MVM) membrane of the STB, whereas MCT4 was predominantly expressed in the MVM but barely detected in the BM. However, obese patients demonstrated significant decreased MCT4 abundance in the MVM coupled with concurrent elevated expression in the BM. We also found a linear trend toward decreasing MCT4 expression ratio of MVM to BM with increasing maternal pre-pregnancy BMI. Furthermore, our data showed that the lactate ratios of fetal cord arterial to maternal blood were remarkably reduced in obese samples compared to their normal counterparts. Collectively, these results suggest that the loss of polarization of lactate transporter MCT4 expression in placental STB leading to disruption of unidirectional lactate transport from the fetal to the maternal compartment may constitute part of mechanisms linking maternal obesity and pathogenesis of stillbirth.
科研通智能强力驱动
Strongly Powered by AbleSci AI