Small Heather Y, Akehurst Christine, Sharafetdinova Liliya, McBride Martin W, McClure John D, Robinson Scott W, Carty David M, Freeman Dilys J, Delles Christian
Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, United Kingdom; and
Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, United Kingdom; and.
Physiol Genomics. 2017 Mar 1;49(3):193-200. doi: 10.1152/physiolgenomics.00106.2016. Epub 2017 Jan 27.
Preeclampsia is a multisystem disease that significantly contributes to maternal and fetal morbidity and mortality. In this study, we used a non-biased microarray approach to identify dysregulated genes in maternal whole blood samples which may be associated with the development of preeclampsia. Whole blood samples were obtained at 28 wk of gestation from 5 women who later developed preeclampsia (cases) and 10 matched women with normotensive pregnancies (controls). Placenta samples were obtained from an independent cohort of 19 women with preeclampsia matched with 19 women with normotensive pregnancies. We studied gene expression profiles using Illumina microarray in blood and validated changes in gene expression in whole blood and placenta tissue by qPCR. We found a transcriptional profile differentiating cases from controls; 336 genes were significantly dysregulated in blood from women who developed preeclampsia. Functional annotation of microarray results indicated that most of the genes found to be dysregulated were involved in inflammatory pathways. While general trends were preserved, only was validated in whole blood samples from cases using qPCR (2.30- ± 0.9-fold change) whereas in placental tissue expression was found to be significantly increased in samples from women with preeclampsia (5.88- ± 2.24-fold change). We have identified that is upregulated in the circulation of women who went on to develop preeclampsia. In placenta of women with preeclampsia we identified that upregulated. Our data provide further evidence for involvement of the gene family in the pathogenesis of preeclampsia.
子痫前期是一种多系统疾病,对孕产妇和胎儿的发病率及死亡率有显著影响。在本研究中,我们采用无偏倚的微阵列方法来鉴定母体全血样本中可能与子痫前期发生相关的失调基因。在妊娠28周时,从5名后来发生子痫前期的女性(病例组)和10名血压正常妊娠的匹配女性(对照组)获取全血样本。胎盘样本来自一个独立队列,其中19名子痫前期女性与19名血压正常妊娠的女性相匹配。我们使用Illumina微阵列研究血液中的基因表达谱,并通过qPCR验证全血和胎盘组织中基因表达的变化。我们发现了一种区分病例组和对照组的转录谱;在发生子痫前期的女性血液中,336个基因显著失调。微阵列结果的功能注释表明,大多数被发现失调的基因参与炎症途径。虽然总体趋势得以保留,但仅在病例组的全血样本中通过qPCR验证了[具体基因](2.30 - ± 0.9倍变化),而在胎盘组织中,子痫前期女性样本中[具体基因]的表达显著增加(5.88 - ± 2.24倍变化)。我们已经确定[具体基因]在后来发生子痫前期的女性循环中上调。在子痫前期女性的胎盘中,我们确定[具体基因]上调。我们的数据为[具体基因]家族参与子痫前期的发病机制提供了进一步的证据。