Objective To study aims to investigate the mechanisms underlying the response of human umbilical vein vascular endothelial cells (HUVECs) to aspirin. Methods HUVECs were treated with or without80ug/mL aspirin for 4 days, and RNA was extracted from HUVECs. After sequencing and data filtering (tool: NGS QC Toolkit), clean data were mapped to genome hg19 (tool: TopHat2). Thereafter, 147differentially expressed genes (DEGs) were identified between aspirin group and control group (tool:Cuffdiff), and DEGs were enriched in 11 pathways associated with cytokine receptor interaction and chemokine signaling. Results Protein-protein interaction network of DEGs was constructed under VEGF stimulation (tool: STRING), and ISG15 and MX1 were hub DEGs. The regulatory network of DEGs and transcription factors (TFs) (tool: TRED database) was also constructed, and CCL2 and FN1 (hub DEGs) were co-regulated by NFKB1 and RELA (hub TFs). Moreover, exon usage and alternative splicing were analyzed (tool: DexSeq) and the splicing of ADORA2A was altered under aspirin stimulation. Conclusion Aspirin might influence HUVECs proliferation and migration, as well as angiogenesis process by regulating the expression of ISG15, MX1, CCL2, FN1 and ADORA2A. However, more research studies are still required to verify these predictions.%目的 旨在探讨潜在的人脐静脉血管内皮细胞(HUVEC)在阿司匹林刺激下的应答机制.方法80μg/mL阿司匹林作用或不作用于人脐静脉血管内皮细胞,4 d后从人脐静脉血管内皮细胞中提取RNA.RNA测序及数据过滤(工具:NGSQC工具包),无异质的数据成图于基因组hg19(工具:tophat2).此后,147个差异表达基因(DEGS)识别于阿司匹林组和对照组之间(工具:cuffdiff),且富集在与细胞因子受体的相互作用和趋化因子信号相关的11条通路上.结果构建差异表达基因蛋白质-蛋白质相互作用网络(工具:STRING),且ISG15和MX1是关键性差异表达基因.构建差异表达基因和转录因子调控网络(TFS)(工具:TRED数据库),CCL2和FN1(枢纽性表达基因)受NFKB1和RELA共同调节(枢纽性TFS).此外,分析外显子的使用和选择性剪接(工具:dexseq),在阿司匹林刺激下ADORA2A剪接发生改变.结论阿司匹林可影响血管内皮细胞的增殖和迁移,可能通过调节ISG15,MX1,CCL2,FN1以及ADORA2A的表达来参与血管生成过程.
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