Beall Marie H, Amidi Fataneh, Gayle Dave A, Wang Shengbiao, Beloosesky Ron, Ross Michael G
Department of Obstetrics and Gynecology, Harbor-UCLA Medical Center and Los Angeles Biomedical Research Institute, Torrance, California 90509, USA.
J Soc Gynecol Investig. 2005 Jul;12(5):298-302. doi: 10.1016/j.jsgi.2005.02.009.
Fetal and amniotic fluid (AF) proteins (eg, alpha fetoprotein [AFP]) are measurable in the maternal circulation. Elevated maternal serum AFP levels indicate a risk for fetal anomalies or for obstetrical complications that are often associated with inflammation (eg, preterm labor). However, little is known of the mechanism of protein exchange between the fetus, AF, and maternal circulation. Nephrin and Neph1 are cell membrane proteins that restrict glomerular protein filtration and which are differentially expressed with renal inflammation. We sought to investigate whether nephrin and Neph1 were expressed in placenta and fetal membranes, and whether inflammation modified the expression.
Pregnant rats at 18 days' gestation were injected with lipopolysacchride (LPS) or control saline intraperitoneally (IP) and killed at 1, 6, and 12 hours after injection. Placenta and fetal membranes were obtained and real-time polymerase chain reaction (PCR) performed for determination of nephrin and Neph1 levels.
Nephrin and Neph1 were expressed in both placenta and fetal membranes. Following maternal LPS administration, nephrin mRNA significantly increased in the membranes (0.22 +/- 0.02 to 0.51 +/- 0.050, P <.05), while Neph1 expression significantly declined in the placenta (0.19 +/- 0.05 to 0.10 +/- 0.01, P <.05).
Fetal membranes and placenta of the rat express mRNA for the protein barriers nephrin and Neph 1, suggesting a role in the regulation of protein transfer from the fetus to mother. Under basal conditions, AF AFP transfer across fetal membranes may account for maternal serum AFP levels, whereas gestational inflammatory conditions (eg, preterm labor, threatened abortion) may augment AFP transfer across the placenta.
胎儿和羊水(AF)中的蛋白质(如甲胎蛋白[AFP])可在母体循环中检测到。母体血清AFP水平升高表明胎儿有异常风险或存在通常与炎症相关的产科并发症(如早产)。然而,对于胎儿、羊水和母体循环之间蛋白质交换的机制知之甚少。Nephrin和Neph1是限制肾小球蛋白质滤过的细胞膜蛋白,且在肾脏炎症时表达存在差异。我们试图研究Nephrin和Neph1是否在胎盘和胎膜中表达,以及炎症是否会改变其表达。
妊娠18天的孕鼠腹腔内注射脂多糖(LPS)或对照生理盐水,注射后1、6和12小时处死。获取胎盘和胎膜,进行实时聚合酶链反应(PCR)以测定Nephrin和Neph1水平。
Nephrin和Neph1在胎盘和胎膜中均有表达。母体给予LPS后,胎膜中Nephrin mRNA显著增加(从0.22±0.02增至0.51±0.050,P<.05),而胎盘中Neph1表达显著下降(从0.19±0.05降至0.10±0.01,P<.05)。
大鼠的胎膜和胎盘表达蛋白质屏障Nephrin和Neph1的mRNA,提示其在调节蛋白质从胎儿向母体转移中起作用。在基础条件下,羊水AFP通过胎膜的转移可能解释母体血清AFP水平,而妊娠炎症状态(如早产、先兆流产)可能增加AFP通过胎盘的转移。