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Abstract：
BACKGROUND: B3GNT7, a glycosyltransferase of significant importance that is highly expressed in intestinal epithelial cells, plays a pivotal role in intestinal physiological processes. This study elucidates novel insights into the potential role and underlying mechanisms of B3GNT7 in ulcerative colitis (UC).
METHODS: An experimental colitis model was induced using DSS in mice to investigate B3GNT7 expression in the colon via transcriptomics and immunohistochemistry. Bioinformatics analysis was employed to delineate the biological functions of B3GNT7. Additionally, the correlation between the transcription levels of B3GNT7 in colonic tissues from patients with UC, sourced from the IBDMDB database, and the severity of colonic inflammation was analyzed to elucidate potential mechanisms.
RESULTS: The DSS-induced colitis model was successfully established, and transcriptomic analysis identified a marked downregulation of B3GNT7 expression in the colonic tissues compared to the controls. Functional enrichment analysis indicated B3GNT7\'s predominant role in mucin O-glycosylation. Protein interaction analysis revealed that B3GNT7 predominantly interacts with members of the mucin MUC family, including MUC2, MUC3, and MUC6. In patients with UC, B3GNT7 transcription levels were significantly reduced, particularly in those with moderate to severe disease activity. The expression level of B3GNT7 exhibited a negative correlation with the endoscopic severity of UC. Gene set enrichment analysis (GSEA) further demonstrated significant enrichment of B3GNT7 in the mucin O-glycosylation synthesis pathway.
CONCLUSIONS: The downregulation of B3GNT7 expression in the colonic tissues of UC patients may contribute to the compromised mucin barrier function and the exacerbation of colitis.
METHODS: An experimental colitis model was induced using DSS in mice to investigate B3GNT7 expression in the colon via transcriptomics and immunohistochemistry. Bioinformatics analysis was employed to delineate the biological functions of B3GNT7. Additionally, the correlation between the transcription levels of B3GNT7 in colonic tissues from patients with UC, sourced from the IBDMDB database, and the severity of colonic inflammation was analyzed to elucidate potential mechanisms.
RESULTS: The DSS-induced colitis model was successfully established, and transcriptomic analysis identified a marked downregulation of B3GNT7 expression in the colonic tissues compared to the controls. Functional enrichment analysis indicated B3GNT7\'s predominant role in mucin O-glycosylation. Protein interaction analysis revealed that B3GNT7 predominantly interacts with members of the mucin MUC family, including MUC2, MUC3, and MUC6. In patients with UC, B3GNT7 transcription levels were significantly reduced, particularly in those with moderate to severe disease activity. The expression level of B3GNT7 exhibited a negative correlation with the endoscopic severity of UC. Gene set enrichment analysis (GSEA) further demonstrated significant enrichment of B3GNT7 in the mucin O-glycosylation synthesis pathway.
CONCLUSIONS: The downregulation of B3GNT7 expression in the colonic tissues of UC patients may contribute to the compromised mucin barrier function and the exacerbation of colitis.
摘要：
背景：B3GNT7，一种重要的糖基转移酶，在肠上皮细胞中高度表达，在肠道生理过程中起着举足轻重的作用。这项研究阐明了B3GNT7在溃疡性结肠炎（UC）中的潜在作用和潜在机制的新见解。
方法：使用DSS在小鼠中诱导实验性结肠炎模型，以通过转录组学和免疫组织化学研究B3GNT7在结肠中的表达。生物信息学分析被用来描述B3GNT7的生物学功能。此外,UC患者结肠组织中B3GNT7转录水平的相关性,来自IBDMDB数据库，并分析结肠炎症的严重程度以阐明潜在的机制。
结果：成功建立DSS诱导的结肠炎模型，和转录组学分析鉴定了与对照相比,结肠组织中B3GNT7表达的显著下调。功能富集分析表明B3GNT7在粘蛋白O-糖基化中的主要作用。蛋白质相互作用分析显示，B3GNT7主要与粘蛋白MUC家族成员相互作用，包括MUC2、MUC3和MUC6。在UC患者中，B3GNT7转录水平显著降低，特别是那些有中度到重度疾病活动的人。B3GNT7的表达水平与UC的严重程度呈负相关。基因集富集分析(GSEA)进一步证明了B3GNT7在粘蛋白O-糖基化合成途径中的显著富集。
结论：UC患者结肠组织中B3GNT7表达下调可能导致粘蛋白屏障功能受损和结肠炎恶化。
方法：使用DSS在小鼠中诱导实验性结肠炎模型，以通过转录组学和免疫组织化学研究B3GNT7在结肠中的表达。生物信息学分析被用来描述B3GNT7的生物学功能。此外,UC患者结肠组织中B3GNT7转录水平的相关性,来自IBDMDB数据库，并分析结肠炎症的严重程度以阐明潜在的机制。
结果：成功建立DSS诱导的结肠炎模型，和转录组学分析鉴定了与对照相比,结肠组织中B3GNT7表达的显著下调。功能富集分析表明B3GNT7在粘蛋白O-糖基化中的主要作用。蛋白质相互作用分析显示，B3GNT7主要与粘蛋白MUC家族成员相互作用，包括MUC2、MUC3和MUC6。在UC患者中，B3GNT7转录水平显著降低，特别是那些有中度到重度疾病活动的人。B3GNT7的表达水平与UC的严重程度呈负相关。基因集富集分析(GSEA)进一步证明了B3GNT7在粘蛋白O-糖基化合成途径中的显著富集。
结论：UC患者结肠组织中B3GNT7表达下调可能导致粘蛋白屏障功能受损和结肠炎恶化。
