Background. This bioinformatics study was aimed to investigate the relationship between periodontitis (PD) and Down Syndrome (DS) regarding potential crosstalk genes, related neuropeptides, and biological processes. Methods. Data for PD (GSE23586, GSE10334 and GSE16134) and DS (GSE35665) were downloaded from NCBI Gene Expression Omnibus (GEO). Following normalization and merging of PD data, differential expression analysis was performed ( value < 0.05 and ). The common deregulated genes between PD and DS were considered as crosstalk genes. The significantly differentially expressed genes were used to construct the coexpression network and to further identify coexpression gene modules. To acquire the significant modules, the significant expression level of genes in the module was used to analyze the enrichment of genes in each module. Neuropeptides were assessed from NeuroPedia database. Neuropeptide genes and crosstalk genes were merged and mapped into PPI network, and the correlation coefficient (Spearman) was determined for the crosstalk genes. Results. 138 crosstalk genes were predicted. According to the functional enrichment analysis, these genes significantly regulated different biological processes and pathways. In enrichment analysis, the significant module of DS was pink module, and turquoise module was significant in PD. Four common crosstalk genes were acquired, i.e., CD19, FCRL5, FCRLA, and HLA-DOB. In the complex network, INS and IGF2 interacted with CASP3 and TP53, which commonly regulated the MAPK signaling pathway. Moreover, the results showed that TP53 interacted with IGF2 and INS inducing the dysregulation of PI3K-Akt signaling pathway. UBL was positively correlated with crosstalk genes in both diseases. LEP was revealed to be both a neuropeptide and crosstalk gene and was positively correlated with other crosstalk genes. Conclusion. Different crosstalk genes, related neuropeptides, and biological pathways and processes were revealed between PD and DS, which can serve as a theoretical basis for future research.

中文翻译：

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神经肽鉴定为转录组学分析揭示的连接唐氏综合症和牙周炎的潜在串扰

背景。这项生物信息学研究旨在调查牙周炎 (PD) 和唐氏综合症 (DS) 之间关于潜在串扰基因、相关神经肽和生物过程的关系。方法。PD（GSE23586、GSE10334 和 GSE16134）和 DS（GSE35665）的数据从 NCBI Gene Expression Omnibus (GEO) 下载。在对 PD 数据进行归一化和合并后，进行差异表达分析（值 < 0.05 和）。PD和DS之间共同的失调基因被认为是串扰基因。将显着差异表达的基因用于构建共表达网络并进一步识别共表达基因模块。为了获得显着模块，模块中基因的显着表达水平用于分析每个模块中基因的富集度。从 NeuroPedia 数据库评估神经肽。将神经肽基因和串扰基因融合并映射到PPI网络中，并确定串扰基因的相关系数（Spearman）。结果. 预测了 138 个串扰基因。根据功能富集分析，这些基因显着调节不同的生物过程和途径。在富集分析中，DS的显着模块是粉色模块，而turquoise模块在PD中是显着的。获得了四种常见的串扰基因，即CD19、FCRL5、FCRLA和HLA-DOB。在复杂网络中，INS 和 IGF2 与 CASP3 和 TP53 相互作用，共同调节 MAPK 信号通路。此外，结果表明TP53与IGF2和INS相互作用，诱导PI3K-Akt信号通路的失调。UBL与两种疾病中的串扰基因呈正相关。LEP被发现既是神经肽又是串扰基因，并且与其他串扰基因呈正相关。结论. 揭示了PD和DS之间不同的串扰基因、相关的神经肽以及生物学通路和过程，可为今后的研究提供理论基础。