Department of Laboratory Medicine, Shanghai Tongji Hospital, School of Medicine, Tongji University, Shanghai 200065, China.
Department of Internal Medicine V-Pulmonology, Allergology, and Respiratory Intensive Care Medicine, Saarland University Hospital, Homburg 66424, Germany.
J Immunol Res. 2022 Jun 25;2022:7280977. doi: 10.1155/2022/7280977. eCollection 2022.
Ulcerative colitis (UC) is an inflammatory bowel disease characterized by persistent colon inflammation. N6-methyladenosine (m6A) methylation is one of the most prevalent RNA modifications with key roles in both normal and illness, but m6A methylation in ulcerative colitis is unknown. This research investigated m6A methylation in UC. We examined the expression of known m6A RNA methylation regulators in UC using the Gene Expression Omnibus database (GEO database). First, we used m6A regulators to examine m6A change in UC samples. These two patient groups were created by clustering three m6A gene expression datasets. These genes were then utilized to build an m6A gene network using WGCNA and PPI. These networks were built using differentially expressed genes. The 12 m6A regulators were found to be dispersed throughout the chromosome. The study's data were then connected, revealing positive or negative relationships between genes or signaling pathways. Then, PCA of the 12 m6A-regulated genes indicated that the two patient groups could be discriminated in both PC1 and PC2 dimensions. The ssGSEA algorithm found that immune invading cells could be easily distinguished across diverse patient groups. Both groups had varied levels of popular cytokines. The differential gene analysis of the two samples yielded 517 genes like FTO and RFX7. It found 9 hub genes among 121 genes in the blue module, compared their expression in two groups of samples, and found that the differences in expression of these 9 genes were highly significant. The identification of 9 possible m6A methylation-dependent gene regulatory networks suggests that m6A methylation is involved in UC pathogenesis. Nine candidate genes have been identified as possible markers for assessing UC severity and developing innovative UC targeted therapeutic approaches.
溃疡性结肠炎（UC）是一种以持续性结肠炎症为特征的炎症性肠病。N6-甲基腺苷（m6A）甲基化是最普遍的 RNA 修饰之一，在正常和疾病中都具有关键作用，但溃疡性结肠炎中的 m6A 甲基化尚不清楚。本研究探讨了 UC 中的 m6A 甲基化。我们使用基因表达综合数据库（GEO 数据库）检查了 UC 中已知 m6A RNA 甲基化调节剂的表达。首先，我们使用 m6A 调节剂检查 UC 样本中的 m6A 变化。这两个患者组是通过聚类三个 m6A 基因表达数据集创建的。然后，我们使用 WGCNA 和 PPI 这些基因构建 m6A 基因网络。这些网络是使用差异表达基因构建的。发现这 12 个 m6A 调节剂分散在整个染色体上。研究的数据然后连接起来，揭示了基因或信号通路之间的正相关或负相关关系。然后，对 12 个 m6A 调节基因的 PCA 分析表明，两个患者组在 PC1 和 PC2 维度上都可以区分。ssGSEA 算法发现，不同患者组之间的免疫浸润细胞可以很容易地区分开来。两组都有不同水平的流行细胞因子。对两个样本的差异基因分析得到了 517 个基因，如 FTO 和 RFX7。在蓝色模块的 121 个基因中发现了 9 个枢纽基因，比较了它们在两组样本中的表达，发现这 9 个基因的表达差异具有高度显著性。鉴定出的 9 个可能的 m6A 甲基化依赖性基因调控网络表明，m6A 甲基化参与了 UC 的发病机制。9 个候选基因被确定为评估 UC 严重程度和开发创新 UC 靶向治疗方法的可能标志物。
