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胎盘lncrna失调与子痫前期的发病机制

Dysregulation of LncRNAs in Placenta and Pathogenesis of Preeclampsia.

作者信息

Song Xuejing, Luo Xiucui, Gao Quansheng, Wang Yuhuan, Gao Qing, Long Wei

机构信息

Department of Obstetrics, Obstetrics and Gynecology Hospital Affiliated to Nanjing Medical University, Nanjing, China.

Department of Obstetrics, Lianyungang Maternity and Child Healthcare Hospital of Jiangsu, Lianyungang 222006, China.

出版信息

Curr Drug Targets. 2017;18(10):1165-1170. doi: 10.2174/1389450118666170404160000.

DOI:10.2174/1389450118666170404160000
PMID:28382860
Abstract

BACKGROUND

Preeclampsia, a gestational disease characterized by hypertension and proteinuria twenty weeks into pregnancy, is one of the leading causes of fetal and maternal mortality. Although multiple genetic and environmental factors are found to be related to the preeclampsia risk, the pathogenic pathways remain largely undefined. The placenta plays a critical role in the fetal development by carrying out the barrier, fetal-maternal exchange, and endocrine functions during pregnancy. Accumulated data indicated that the expression of multiple long noncoding RNA (LncRNA) is dysregulated in preeclamptic placentas. Moreover, manipulation of LncRNA expression led to functional alterations in trophoblast cell cultures, including changes in proliferation, differentiation, apoptosis, and migration.

OBJECTIVE

This article reviews published data on this subject and provides detailed information on the regulation and function of LncRNAs IGF2/H19, MEG3, SPRY4-IT1, HOTAIR, MALAT1, and FLT1P1 and CEACAMP8 in placental trophoblasts. The potential mechanisms underlying the action of these LncRNAs are also discussed to facilitate a better understanding on the potential role of these LncRNAs for the pathogenesis of preeclampsia.

CONCLUSION

It is elaborated that some lncRNAs probably contribute to the pathogenesis of preeclampsia through methylation, Notch-EGFL7 signaling pathway and Wnt/β-catenin pathway.

摘要

背景

子痫前期是一种妊娠疾病,其特征为妊娠20周后出现高血压和蛋白尿,是导致胎儿和孕产妇死亡的主要原因之一。尽管发现多种遗传和环境因素与子痫前期风险相关,但其致病途径仍 largely 未明确。胎盘在孕期通过执行屏障、胎儿-母体交换和内分泌功能,在胎儿发育中发挥关键作用。累积数据表明,多种长链非编码RNA(LncRNA)在子痫前期胎盘组织中的表达失调。此外,对LncRNA表达的操控导致滋养层细胞培养物出现功能改变,包括增殖、分化、凋亡和迁移的变化。

目的

本文回顾了关于该主题已发表的数据,并提供了关于LncRNAs IGF2/H19、MEG3、SPRY4-IT1、HOTAIR、MALAT1、FLT1P1以及CEACAMP8在胎盘滋养层细胞中的调控和功能的详细信息。还讨论了这些LncRNAs发挥作用的潜在机制,以促进更好地理解这些LncRNAs在子痫前期发病机制中的潜在作用。

结论

阐述了一些lncRNAs可能通过甲基化、Notch-EGFL7信号通路和Wnt/β-连环蛋白通路参与子痫前期的发病机制。

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