PDF(Pubmed)
Abstract：
Ulcerative colitis (UC) is a chronic inflammatory disease that targets the colon and has seen an increasing prevalence worldwide. In our pursuit of new diagnostic and therapeutic approaches for UC, we undertook a sequencing of colons from UC mouse models. We focused on analyzing their differentially expressed genes (DEGs), enriching pathways, and constructing protein-protein interaction (PPI) and Competing Endogenous RNA (ceRNA) networks. Our analysis highlighted novel DEGs such as Tppp3, Saa3, Cemip, Pappa, and Nr1d1. These DEGs predominantly play roles in pathways like cytokine-mediated signaling, extracellular matrix organization, extracellular structure organization, and external encapsulating structure organization. This suggests that the UC pathogenesis is intricately linked to the interactions between immune and non-immune cells with the extracellular matrix (ECM). To corroborate our findings, we also verified certain DEGs through quantitative real-time PCR. Within the PPI network, nodes like Stat3, Il1b, Mmp3, and Lgals3 emerged as significant and were identified to be involved in the crucial cytokine-mediated signaling pathway, which is central to inflammation. Our ceRNA network analysis further brought to light the role of the Smad7 Long non-coding RNA (lncRNA). Key MicroRNA (miRNAs) in the ceRNA network were pinpointed as mmu-miR-17-5p, mmu-miR-93-5p, mmu-miR-20b-5p, mmu-miR-16-5p, and mmu-miR-106a-5p, while central mRNAs included Egln3, Plagl2, Sema7a, Arrdc3, and Stat3. These insights imply that ceRNA networks are influential in UC progression and could provide further clarity on its pathogenesis. In conclusion, this research deepens our understanding of UC pathogenesis and paves the way for potential new diagnostic and therapeutic methods. Nevertheless, to solidify our findings, additional experiments are essential to confirm the roles and molecular interplay of the identified DEGs in UC.
摘要：
溃疡性结肠炎（UC）是一种以结肠为目标的慢性炎症性疾病，并且在全球范围内的患病率越来越高。在我们寻求UC新的诊断和治疗方法的过程中，我们对UC小鼠模型的结肠进行了测序。我们专注于分析它们的差异表达基因(DEG)，丰富的途径，构建蛋白质-蛋白质相互作用（PPI）和竞争内源性RNA（ceRNA）网络。我们的分析突出了新颖的DEG，如Tppp3，Saa3，Cemip，Pappa,和Nr1d1。这些DEGs主要在细胞因子介导的信号通路中发挥作用，细胞外基质组织，细胞外结构组织，和外部封装结构组织。这表明UC发病机理与免疫细胞和非免疫细胞与细胞外基质(ECM)之间的相互作用密切相关。为了证实我们的发现，我们还通过定量实时PCR验证了某些DEGs。在PPI网络中，像Stat3、Il1b、Mmp3和Lgals3具有重要意义，并被确定参与关键的细胞因子介导的信号通路，这是炎症的核心。我们的ceRNA网络分析进一步揭示了Smad7长非编码RNA（lncRNA）的作用。CERNA网络中的关键MicroRNA（miRNA）被确定为mmu-miR-17-5p，mmu-miR-93-5p，mmu-miR-20b-5p，mmu-miR-16-5p，和mmu-miR-106a-5p，而中央mRNA包括Egln3，Plagl2，Sema7a，Arrdc3和Stat3。这些见解意味着ceRNA网络对UC进展有影响，并且可以进一步阐明其发病机理。总之,这项研究加深了我们对UC发病机制的理解,为潜在的新诊断和治疗方法铺平了道路.然而，巩固我们的发现，另外的实验对于确认已鉴定的DEGs在UC中的作用和分子相互作用是必不可少的.
