牙髓炎的发病机制和分子靶标研究

Study on the pathogenesis and molecular target of pulpitis

目的鉴定牙髓炎的发病机制和分子靶标。方法通过GEO数据GSE77459 (2016年2月)和GSE92681(2017年12月)确定牙髓炎组织中的差异表达基因。富集分析和基因集富集分析深入评价差异基因在牙髓炎过程中的作用机制。通过PPI网络和分子实验鉴定出牙髓炎相关的关键因子。结果在GSE77459数据的牙髓炎组织中发现了1280个差异表达基因(DEGs)。经过GSE92681数据集验证到81个DEGs。富集分析和基因集富集分析发现DEGs与免疫及炎症反应显著相关。PPI网络分析筛选了55个网络基因,并识别出CD44为核心网络因子和调控基因。通过实时定量聚合酶链反应和Western blot验证了CD44在牙髓炎组织中显著表达上调。结论 CD44是牙髓炎的潜在生物标志物及治疗靶标,并通过ERK1/2信号通路参与到牙髓炎的发展过程中。

Objective To identify the pathogenesis and molecular target of pulpitis. Methods Differentially expressed genes in pulpitis tissue were identified by GEO data GSE77459(February 2016) and GSE92681(December 2017). Enrichment analysis and gene set enrichment analysis were used to evaluate the mechanism of differential genes in pulpitis. The key factors associated with pulpitis were identified by PPI network and molecular experiments. Results There were 1280 differentially expressed genes(DEGs) were identified in pulpitis tissue from GSE77459 data. Eighty-one DEGs were verified by GSE92681 data set. Enrichment analysis and gene set enrichment analysis showed that DEGs was significantly correlated with immune and inflammatory responses. PPI network analysis screened 55 network genes and identified CD44 as the core network factor and regulatory gene. The expression of CD44 in pulpitis tissue was significantly up-regulated by real-time quantitative polymerase chain reaction and Western blot analysis. Conclusion CD44 is a potential biomarker and therapeutic target for pulpitis and is involved in the development of pulpitis through the ERK1/2 signaling pathway.