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Comprehensive microarray analysis of severe preeclampsia placenta to identify differentially expressed genes, biological pathways, hub genes, and their related non-coding RNAs
Placenta ( IF 3.0 ) Pub Date : 2024-08-06 , DOI: 10.1016/j.placenta.2024.08.003
Maedeh Shabani 1 , Maryam Eghbali 2 , Ameneh Abiri 3 , Maryam Abiri 4
Affiliation  

Preeclampsia (PE) is a serious pregnancy-related complication caused by high blood pressure in pregnant women. The severe form has more devastating effects. According to the growing evidence, the placenta is a crucial component in the pathogenesis of PE, and eliminating it will alleviate symptoms. GEO's severe preeclampsia placenta microarray datasets; GSE147776, GSE66273, GSE102897, and GSE10588, were chosen to identify differentially expressed genes (DEGs) in different biological pathways. The analysis of hub genes and related non-coding RNAs was done as well. A total of 347 DEGs with adj p-value <0.05 and ǀlog2FoldChangeǀ> 0.5 were discovered between severe PEs and healthy pregnancies, including 204 over-expressed genes and 143 under-expressed genes. The MCC method identified genes as the top ten hub genes. Interactions between hub genes and noncoding RNAs were also conducted. The most enriched pathways were as follows; HIF-1 signaling pathway; Pathways in cancer; Alanine, aspartate and glutamate metabolism; Arginine biosynthesis; Human papillomavirus infection; Glycolysis/Gluconeogenesis; Central carbon metabolism in cancer; Valine, leucine and isoleucine degradation; Cysteine and methionine metabolism; and Galactose metabolism. This is a secondary data analysis conducted on severe preeclampsia placenta to identify differentially expressed genes, biological pathways, hub-genes, and related noncoding RNAs. Functional studies are crucial to understanding the precise role of these genes in the pathogenesis of PE. Also, accepting a gene as a diagnostic or prognostic marker for early diagnosis and management of PE requires multiple lines of evidence.

中文翻译:


对重度子痫前期胎盘进行全面的微阵列分析,以确定差异表达基因、生物学途径、枢纽基因及其相关非编码RNA



先兆子痫(PE)是孕妇高血压引起的严重妊娠相关并发症。严重的形式具有更具破坏性的影响。越来越多的证据表明,胎盘是 PE 发病机制的重要组成部分,消除胎盘可以缓解症状。 GEO 的重度先兆子痫胎盘微阵列数据集;选择 GSE147776、GSE66273、GSE102897 和 GSE10588 来识别不同生物途径中的差异表达基因 (DEG)。还进行了 hub 基因和相关非编码 RNA 的分析。在严重PE和健康妊娠之间总共发现了347个ADJ p值<0.05和ǀlog2FoldChangeǀ> 0.5的DEG,其中包括204个过度表达的基因和143个表达不足的基因。 MCC方法将基因确定为前十名枢纽基因。还进行了 hub 基因和非编码 RNA 之间的相互作用。最富集的途径如下: HIF-1信号通路;癌症的途径;丙氨酸、天冬氨酸和谷氨酸代谢;精氨酸生物合成;人乳头瘤病毒感染;糖酵解/糖异生;癌症中的中心碳代谢;缬氨酸、亮氨酸和异亮氨酸降解;半胱氨酸和蛋氨酸代谢;和半乳糖代谢。这是对严重先兆子痫胎盘进行的二次数据分析,旨在识别差异表达基因、生物途径、中枢基因和相关非编码 RNA。功能研究对于了解这些基因在 PE 发病机制中的确切作用至关重要。此外,接受基因作为 PE 早期诊断和治疗的诊断或预后标记需要多方面的证据。
更新日期:2024-08-06
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