Li Na, Hou Rui, Liu Caixia, Yang Tian, Qiao Chong, Wei Jun
Department of Obstetrics and Gynecology, Shengjing Hospital of China Medical University, Shenyang, China.
Key Laboratory of Maternal-Fetal Medicine of Liaoning Province; Key Laboratory of Obstetrics and Gynecology of Higher Education of Liaoning Province, Benxi, China.
Clin Proteomics. 2021 Dec 29;18(1):31. doi: 10.1186/s12014-021-09336-8.
Placenta accreta (PA) is a major cause of maternal morbidity and mortality in modern obstetrics, few studies have explored the underlying molecular mechanisms.
In our study, transcriptome and proteome profiling were performed in placental tissues from ten participants including five cases each in the PA and control groups to clarify the pathogenesis of PA.
We identified differential expression of 37,743 transcripts and 160 proteins between the PA and control groups with an overlap rate of 0.09%. The 33 most-significant transcripts and proteins were found and further screened and analyzed. Adhesion-related signature, chemotaxis related signatures and immune related signature were found in the PA group and played a certain role. Sum up two points, three significant indicators, methyl-CpG-binding domain protein 2 (MeCP2), podocin (PODN), and apolipoprotein D (ApoD), which participate in "negative regulation of cell migration", were downregulated at the mRNA and protein levels in PA group. Furthermore, transwell migration and invasion assay of HTR-8/SVneo cell indicated the all of them impaired the migration and invasion of trophoblast.
A poor correlation was observed between the transcriptome and proteome data and MeCP2, PODN, and ApoD decreased in transcriptome and proteome profiling, resulting in increased migration of trophoblasts in the PA group, which clarify the mechanism of PA and might be the biomarkers or therapy targets in the future.
胎盘植入（PA）是现代产科孕产妇发病和死亡的主要原因，很少有研究探讨其潜在的分子机制。
在我们的研究中，对10名参与者的胎盘组织进行了转录组和蛋白质组分析，其中PA组和对照组各5例，以阐明PA的发病机制。
我们发现PA组和对照组之间有37,743个转录本和160种蛋白质存在差异表达，重叠率为0.09%。我们找到了33个最显著的转录本和蛋白质，并进一步进行筛选和分析。在PA组中发现了与黏附相关的特征、趋化相关特征和免疫相关特征，并发挥了一定作用。总结两点，三个显著指标，即参与“细胞迁移的负调控”的甲基化CpG结合域蛋白2（MeCP2）、足突蛋白（PODN）和载脂蛋白D（ApoD），在PA组的mRNA和蛋白质水平均下调。此外，HTR-8/SVneo细胞的Transwell迁移和侵袭试验表明，它们均损害了滋养层细胞的迁移和侵袭。
转录组和蛋白质组数据之间相关性较差，且在转录组和蛋白质组分析中MeCP2、PODN和ApoD减少，导致PA组中滋养层细胞迁移增加，这阐明了PA的机制，可能是未来的生物标志物或治疗靶点。
