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通过转录组分析鉴定唐氏综合征和牙周炎之间潜在的神经肽串扰。

Identification of Neuropeptides as Potential Crosstalks Linking Down Syndrome and Periodontitis Revealed by Transcriptomic Analyses.

机构信息

Department of Pediatrics, Shanghai East Hospital, Tongji University School of Medicine, Shanghai 200120, China.

Department of Medical Oncology, Shanghai Pulmonary Hospital, Thoracic Cancer Institute, Tongji University School of Medicine, Shanghai 200433, China.

出版信息

Dis Markers. 2021 Sep 10;2021:7331821. doi: 10.1155/2021/7331821. eCollection 2021.

DOI:10.1155/2021/7331821
PMID:34545294
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8449741/
Abstract

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 ∣log FC | ≥0.5). 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.

摘要

背景

本生物信息学研究旨在探讨牙周炎(PD)和唐氏综合征(DS)之间的潜在串扰基因、相关神经肽和生物学过程的关系。

方法

从 NCBI 基因表达综合数据库(GEO)下载 PD(GSE23586、GSE10334 和 GSE16134)和 DS(GSE35665)的数据。对 PD 数据进行归一化和合并后,进行差异表达分析( 值 < 0.05,∣logFC∣≥0.5)。将 PD 和 DS 之间共同失调的基因视为串扰基因。显著差异表达的基因用于构建共表达网络,并进一步鉴定共表达基因模块。为了获得显著模块,使用模块中基因的显著表达水平分析每个模块中基因的富集情况。从 NeuroPedia 数据库中评估神经肽。将神经肽基因和串扰基因合并并映射到 PPI 网络中,并确定串扰基因的相关系数(Spearman)。

结果

预测出 138 个串扰基因。根据功能富集分析,这些基因显著调节了不同的生物学过程和途径。在富集分析中,DS 的显著模块为粉色模块,PD 的显著模块为绿松石模块。获得了四个共同的串扰基因,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,导致 PI3K-Akt 信号通路失调。UBL 在两种疾病中与串扰基因呈正相关。LEP 既是神经肽又是串扰基因,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、相关神经肽以及生物学途径和过程,可为未来的研究提供理论依据。

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