Department of Orthopedics, Affiliated Hospital of Putian University, Putian, Fujian, China
Department of Gastroenterological Surgery, Affiliated Hospital of Putian University, Putian, Fujian, China
Turk J Gastroenterol. 2023 May;34(5):490-496. doi: 10.5152/tjg.2023.22572.
Alternative splicing of pre-messenger RNA is recognized as the crucial mechanism for gene expression regulation and proteome diversity generation. Alternative splicing has been found to be related to the pathogenesis of inflammatory bowel disease. The aim of this study was to identify the alternative splicing events in intestinal epithelial cells from mouse models of acute colitis and expand the understanding of the pathogenesis of inflammatory bowel disease.
The acute colitis mouse models were constructed, and intestinal epithelial cells of the colon were isolated for RNA sequence. The replicate Multivariate Analysis of Transcript Splicing software was used to analyze the alternative splicing events. The functional analysis was performed on genes with significant differential alternative splicing events. The alternative splicing events of picked genes were validated by reverse transcription polymerase chain reaction.
A total of 340 significant differential alternative splicing events (from 293 genes) were screened out in acute colitis, and the alternative splicing events of CDK5-regulatory subunit associated protein 3 and TRM5 tRNA methyltransferase 5 were validated. The functional analysis showed that differential alternative splicing events in acute colitis participate in the apoptotic process, and the alternative splicing events of 3 genes (BCL2/adenovirus E1B-interacting protein 2, tumor necrosis factor receptor-associated factor 1, and tumor necrosis factor receptor-associated factor 7) were validated by reverse transcription polymerase chain reaction.
This study pointed out the potential impact of different alternative splicing in acute colitis.
前信使 RNA 的可变剪接被认为是基因表达调控和蛋白质组多样性产生的关键机制。可变剪接已被发现与炎症性肠病的发病机制有关。本研究旨在鉴定急性结肠炎小鼠模型肠道上皮细胞中的可变剪接事件，以扩展对炎症性肠病发病机制的认识。
构建急性结肠炎小鼠模型，分离结肠肠道上皮细胞进行 RNA 测序。使用复制多元分析转录剪接软件分析可变剪接事件。对具有显著差异可变剪接事件的基因进行功能分析。通过逆转录聚合酶链反应验证所选基因的可变剪接事件。
在急性结肠炎中筛选出 340 个显著差异可变剪接事件（来自 293 个基因），并验证了 CDK5 调节亚基相关蛋白 3 和 TRM5 tRNA 甲基转移酶 5 的可变剪接事件。功能分析表明，急性结肠炎中的差异可变剪接事件参与细胞凋亡过程，通过逆转录聚合酶链反应验证了 3 个基因（BCL2/腺病毒 E1B 相互作用蛋白 2、肿瘤坏死因子受体相关因子 1 和肿瘤坏死因子受体相关因子 7）的可变剪接事件。
本研究指出了不同可变剪接在急性结肠炎中的潜在影响。
