Scioscia Marco, Gumaa Khalid, Whitten Melissa, Selvaggi Luigi E, Rodeck Charles H, Rademacher Thomas W
Department of Immunology and Molecular Pathology, Molecular Medicine Unit, Royal Free and University College London Medical School, London, UK.
J Reprod Immunol. 2007 Dec;76(1-2):85-90. doi: 10.1016/j.jri.2007.03.016. Epub 2007 May 9.
An association between inositol phosphoglycan P-type (P-IPG) and preeclampsia has been demonstrated over recent years. This molecule can mediate many of the metabolic and growth promoting effects of insulin. Dysregulation of the mediator family is associated with insulin resistance. An increased concentration of P-IPG has been reported in preeclamptic placenta, although its precursor (GPI) was undetectable in those placental samples. Insulin administration, that induces P-IPG release in normal human placenta, was shown not to cause production/release of the mediator from preeclamptic placental tissue as a consequence of a disturbed insulin signalling. Amniotic fluid is enriched of this mediator, with further increase during preeclampsia. We have found that the fetus released increasing amounts of P-IPG in the urine between 13 and 18 weeks of gestation, reaching a plateau beyond 20 weeks. Cord blood of infants of preeclamptic mothers showed an increased content of soluble P-IPG compared to controls and to the mother.
近年来，已证实肌醇磷酸聚糖P型（P-IPG）与先兆子痫之间存在关联。该分子可介导胰岛素的许多代谢和促生长作用。介质家族的失调与胰岛素抵抗有关。尽管在子痫前期胎盘样本中未检测到其前体（GPI），但子痫前期胎盘中P-IPG的浓度有所升高。在正常人体胎盘中诱导P-IPG释放的胰岛素给药，由于胰岛素信号传导紊乱，并未导致子痫前期胎盘组织产生/释放该介质。羊水富含这种介质，子痫前期时会进一步增加。我们发现，胎儿在妊娠13至18周期间尿液中释放的P-IPG量不断增加，20周后达到平台期。与对照组和母亲相比，子痫前期母亲所生婴儿的脐血中可溶性P-IPG含量增加。
