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子痫前期对母胎界面基因表达的影响。

The Impact of Preeclampsia on Gene Expression at the Maternal-Fetal Interface.

作者信息

Winn Virginia D, Gormley Matthew, Fisher Susan J

机构信息

Department of Obstetrics and Gynecology, University of Colorado School of Medicine, Aurora, Colorado 80045.

出版信息

Pregnancy Hypertens. 2011 Jan 1;1(1):100-8. doi: 10.1016/j.preghy.2010.12.001.

DOI:10.1016/j.preghy.2010.12.001
PMID:21743843
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3129988/
Abstract

Preeclampsia (PE) impacts 8 million mother-infant pairs worldwide each year. This human pregnancy-specific disease characterized by hypertension and proteinuria accounts for significant maternal and neonatal morbidity and mortality. The current theory of the pathogenesis of PE as reviewed by Drs. Christopher Redman and Ian Sargent is thought to occur as a 2-stage process with poor placentation in the first half of pregnancy resulting in the maternal response in the second half of pregnancy. Our studies have focused on understanding the placental contribution to this serious disease by examining the gene expression profile of the deciduas basalis or basal plate, the region of the placenta involved in the "poor placentation". In this review we present summaries of our microarray datasets both of normal placentation and those gene expression changes resulting in the context of PE. Additionally, we have taken this opportunity to combine the data sets to provide a more comprehensive view of this region of the placenta. As defects in the basal plate are, in part, at the root of the disease process, we believe that understanding the pathobiology that occurs in this region will increase our ability to alter the development and/or course of PE.

摘要

子痫前期(PE)每年影响全球800万母婴。这种以高血压和蛋白尿为特征的人类妊娠期特有疾病导致了严重的孕产妇和新生儿发病及死亡。克里斯托弗·雷德曼博士和伊恩·萨金特博士综述的当前PE发病机制理论认为,其发生过程分为两个阶段,妊娠前半期胎盘形成不良,导致妊娠后半期母体产生反应。我们的研究重点是通过检查基蜕膜或基底板(胎盘参与“胎盘形成不良”的区域)的基因表达谱,来了解胎盘对这种严重疾病的影响。在这篇综述中,我们展示了正常胎盘形成以及PE情况下基因表达变化的微阵列数据集摘要。此外,我们借此机会合并数据集,以更全面地了解胎盘的这个区域。由于基底板的缺陷部分是疾病过程的根源,我们相信了解该区域发生的病理生物学将提高我们改变PE发展和/或病程的能力。

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本文引用的文献

1
Severe preeclampsia-related changes in gene expression at the maternal-fetal interface include sialic acid-binding immunoglobulin-like lectin-6 and pappalysin-2.重度子痫前期相关的母胎界面基因表达变化包括唾液酸结合免疫球蛋白样凝集素-6和妊娠相关血浆蛋白A2。
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Human-specific expression of Siglec-6 in the placenta.Siglec-6在胎盘中的人类特异性表达。
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Gene expression profiling of the human maternal-fetal interface reveals dramatic changes between midgestation and term.人类母胎界面的基因表达谱分析揭示了妊娠中期和足月之间的显著变化。
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Soluble endoglin and other circulating antiangiogenic factors in preeclampsia.子痫前期中的可溶性内皮糖蛋白及其他循环抗血管生成因子。
N Engl J Med. 2006 Sep 7;355(10):992-1005. doi: 10.1056/NEJMoa055352.
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Serum adiponectin, leptin and soluble leptin receptor in pre-eclampsia.子痫前期患者血清脂联素、瘦素及可溶性瘦素受体水平
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Relationships between maternal plasma leptin, placental leptin mRNA and protein in normal pregnancy, pre-eclampsia and intrauterine growth restriction without pre-eclampsia.正常妊娠、子痫前期及无子痫前期的胎儿生长受限孕妇血浆瘦素、胎盘瘦素mRNA和蛋白之间的关系。
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Microcephalin, a gene regulating brain size, continues to evolve adaptively in humans.小头畸形基因,一种调节脑容量的基因,在人类中继续进行适应性进化。
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