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使用全基因组微阵列对血管阻力增加的胎盘和子痫前期进行差异基因表达分析。

Differential gene expression analysis of placentas with increased vascular resistance and pre-eclampsia using whole-genome microarrays.

作者信息

Centlow M, Wingren C, Borrebaeck C, Brownstein M J, Hansson S R

机构信息

Departments of Obstetrics and Gynecology and Clinical Sciences, Lund University, BMC C14, Klinikgatan 28, 221 84 Lund, Sweden.

出版信息

J Pregnancy. 2011;2011:472354. doi: 10.1155/2011/472354. Epub 2011 Mar 8.

DOI:10.1155/2011/472354
PMID:21490790
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3066560/
Abstract

Pre-eclampsia is a pregnancy complication characterized by hypertension and proteinuria. There are several factors associated with an increased risk of developing pre-eclampsia, one of which is increased uterine artery resistance, referred to as "notching". However, some women do not progress into pre-eclampsia whereas others may have a higher risk of doing so. The placenta, central in pre-eclampsia pathology, may express genes associated with either protection or progression into pre-eclampsia. In order to search for genes associated with protection or progression, whole-genome profiling was performed. Placental tissue from 15 controls, 10 pre-eclamptic, 5 pre-eclampsia with notching, and 5 with notching only were analyzed using microarray and antibody microarrays to study some of the same gene product and functionally related ones. The microarray showed 148 genes to be significantly altered between the four groups. In the preeclamptic group compared to notch only, there was increased expression of genes related to chemotaxis and the NF-kappa B pathway and decreased expression of genes related to antigen processing and presentation, such as human leukocyte antigen B. Our results indicate that progression of pre-eclampsia from notching may involve the development of inflammation. Increased expression of antigen-presenting genes, as seen in the notch-only placenta, may prevent this inflammatory response and, thereby, protect the patient from developing pre-eclampsia.

摘要

子痫前期是一种以高血压和蛋白尿为特征的妊娠并发症。有几个因素与子痫前期发生风险增加相关,其中之一是子宫动脉阻力增加,即所谓的“切迹”。然而,一些女性不会发展为子痫前期,而另一些女性则有更高的发病风险。胎盘在子痫前期病理过程中起核心作用,可能表达与子痫前期保护或进展相关的基因。为了寻找与保护或进展相关的基因,进行了全基因组分析。使用微阵列和抗体微阵列分析了15名对照者、10名单纯子痫前期患者、5名伴有切迹的子痫前期患者以及5名仅有切迹患者的胎盘组织,以研究一些相同的基因产物及其功能相关基因。微阵列显示四组之间有148个基因发生了显著改变。与仅有切迹组相比,子痫前期组中与趋化作用和核因子κB途径相关的基因表达增加,而与抗原加工和呈递相关的基因表达减少,如人类白细胞抗原B。我们的结果表明,从切迹发展为子痫前期可能涉及炎症的发生。如在仅有切迹的胎盘中所见,抗原呈递基因表达增加可能会阻止这种炎症反应,从而保护患者不发展为子痫前期。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efd5/3066560/768fe6c3744f/JP2011-472354.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efd5/3066560/fa9e7105beb8/JP2011-472354.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efd5/3066560/b788888693ca/JP2011-472354.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efd5/3066560/768fe6c3744f/JP2011-472354.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efd5/3066560/fa9e7105beb8/JP2011-472354.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efd5/3066560/b788888693ca/JP2011-472354.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efd5/3066560/768fe6c3744f/JP2011-472354.003.jpg

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