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鉴定和综合分析与人类牙周炎相关的差异表达长非编码 RNA。

Identification and integrated analysis of differentially expressed long non-coding RNAs associated with periodontitis in humans.

机构信息

Orthodontics, Faculty of Dentistry, the University of Hong Kong, Hong Kong SAR.

Periodontology & Implant Dentistry, Faculty of Dentistry, the University of Hong Kong, Hong Kong SAR.

出版信息

J Periodontal Res. 2021 Aug;56(4):679-689. doi: 10.1111/jre.12864. Epub 2021 Mar 9.

DOI:10.1111/jre.12864
PMID:33751610
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8359208/
Abstract

BACKGROUND AND OBJECTIVE

Long non-coding RNAs (lncRNAs) can act as competing endogenous RNAs (ceRNAs) to compete for micro-RNAs (miRNAs) in regulation of downstream genes, various biological functions and diseases. Yet, the expression and regulation of lncRNAs in periodontitis are not fully understood. The objective of the study was to identify potential genes (lncRNA, messenger RNA [mRNA] and miRNA) involved in periodontitis, construct lncRNA-miRNA-mRNA ceRNA networks, explore gene functions and validate gene expressions.

MATERIAL AND METHODS

The data sets for the lncRNA, mRNA and miRNA expression profiles in gingival samples from periodontally healthy subjects and chronic periodontitis patients were obtained from the Gene Expression Omnibus. The differentially expressed lncRNAs (DElncRNAs), mRNAs (DEmRNAs) and miRNAs (DEmiRNAs) were identified, and ceRNA networks were then constructed. The expression of DElncRNAs and DEmRNAs was examined by quantitative real-time polymerase chain reaction (qPCR). Moreover, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were performed for exploring the potential functions and biological pathways.

RESULTS

The GSE80715 and GSE54710 data sets were retrieved. Subsequently, 26 DElncRNAs, 436 DEmRNAs and 12 DEmiRNAs were identified (|fold change| ≥2, adjusted p < 0.05). Further bioinformatics analysis contributed to establishment of the ceRNA networks, which consisted of 10 DElncRNAs, 11 DEmiRNAs and 83 DEmRNAs. Notably, the qPCR results showed a marked decrease in the expression of lncRNA H19 and two mRNAs (NOS1 and MAPT) which further supported the identified ceRNA network. The GO results revealed that the up-regulated mRNAs were significantly enriched in inflammatory processes, whilst the down-regulated mRNAs were enriched in cellular potentials.

CONCLUSION

Non-coding RNAs are critically involved in the regulatory mechanisms in the pathogenesis of periodontitis. Further study is warranted to investigate the specific underlying genetic traits and networks.

摘要

背景与目的

长链非编码 RNA(lncRNA)可以作为竞争性内源 RNA(ceRNA)与 microRNA(miRNA)竞争,从而调控下游基因的表达,具有多种生物学功能并与多种疾病相关。然而,lncRNA 在牙周炎中的表达和调控尚不完全清楚。本研究旨在鉴定参与牙周炎的潜在基因(lncRNA、信使 RNA [mRNA] 和 miRNA),构建 lncRNA-miRNA-mRNA ceRNA 网络,探讨基因功能并验证基因表达。

材料与方法

从基因表达综合数据库(GEO)中获取牙周健康受试者和慢性牙周炎患者牙龈组织的 lncRNA、mRNA 和 miRNA 表达谱数据集。筛选差异表达的 lncRNA(DElncRNA)、mRNA(DEmRNA)和 miRNA(DEmiRNA),构建 ceRNA 网络。采用实时定量聚合酶链反应(qPCR)检测 DElncRNA 和 DEmRNA 的表达。此外,还进行了基因本体(GO)和京都基因与基因组百科全书(KEGG)通路富集分析,以探讨潜在的功能和生物学途径。

结果

共检索到 GSE80715 和 GSE54710 数据集。进一步分析筛选出 26 个 DElncRNA、436 个 DEmRNA 和 12 个 DEmiRNA(|fold change| ≥2,调整 p<0.05)。进一步的生物信息学分析有助于建立 ceRNA 网络,该网络由 10 个 DElncRNA、11 个 DEmiRNA 和 83 个 DEmRNA 组成。值得注意的是,qPCR 结果显示 lncRNA H19 和两个 mRNAs(NOS1 和 MAPT)的表达明显下降,进一步支持了所鉴定的 ceRNA 网络。GO 结果表明,上调的 mRNAs 显著富集于炎症过程,而下调的 mRNAs 则富集于细胞潜能。

结论

非编码 RNA 参与了牙周炎发病机制中的调控机制。需要进一步研究以探讨特定的遗传特征和网络。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6ca/8359208/b7a95bce1793/JRE-56-679-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6ca/8359208/ee003252e07f/JRE-56-679-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6ca/8359208/5c87fc8faf5b/JRE-56-679-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6ca/8359208/545945fc022d/JRE-56-679-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6ca/8359208/b7a95bce1793/JRE-56-679-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6ca/8359208/ee003252e07f/JRE-56-679-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6ca/8359208/5c87fc8faf5b/JRE-56-679-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6ca/8359208/545945fc022d/JRE-56-679-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6ca/8359208/b7a95bce1793/JRE-56-679-g002.jpg

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