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循环 miRNA 作为牙周炎与子痫前期关联的表观遗传介质。

Circulating miRNAs as Epigenetic Mediators of Periodontitis and Preeclampsia Association.

机构信息

Department of Obstetrics, The Affiliated Tai'an City Central Hospital of Qingdao University, Tai'an, 271000 Shandong Province, China.

Department of Stomatology, The Affiliated Tai'an City Central Hospital of Qingdao University, Tai'an, 271000 Shandong Province, China.

出版信息

Dis Markers. 2022 Jul 11;2022:2771492. doi: 10.1155/2022/2771492. eCollection 2022.

DOI:10.1155/2022/2771492
PMID:35860693
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9293528/
Abstract

OBJECTIVE

Periodontal disease has been associated with pregnancy complications including preeclampsia. This bioinformatic study is aimed at investigating the possible role of circulating microRNAs (miRNAs) as mediators of the association between maternal periodontal disease and preeclampsia.

METHODS

Peripheral blood miRNA profiles of periodontitis and controls were sought from Gene Expression Omnibus (GEO), and differential expression analysis was performed. Experimentally validated circulating miRNAs associated with preeclampsia were determined from the Human MicroRNA Disease Database (HMDD v3.0). Venn diagrams were drawn to identify shared circulating differential miRNAs (DEmiRNAs). Significantly enriched target genes, KEGG pathways, and Gene Ontology (GO) terms for the set of shared DEmiRNA were predicted using miRNA enrichment analysis and annotation tool (miEAA v 2.0). Additionally, the shared DEmiRNA-enriched target genes were analyzed for enriched WikiPathways, BioCarta metabolic pathways, and tissue proteins in the human proteome map.

RESULTS

Among 183 circulating DEmiRNA in periodontitis and 60 experimentally validated miRNA in preeclampsia, 9 shared DEmiRNA were identified. The top among 32 overrepresented target genes included MAFB, PSAP, and CDK5RAP2, top among 14 enriched KEGG pathways were renin-angiotensin system and graft-versus-host disease, and that among enriched 44 GO profiles included "positive regulation of epidermal growth factor-activated receptor activity" and "sequestering of calcium ion." In the overrepresented target gene set, among 10 enriched WikiPathways, the top included "NAD metabolism, sirtuins, and aging" and "regulation of Wnt/B-catenin signaling by small molecule compounds" and PPAR-related mechanisms was top among 13 enriched BioCarta metabolic pathways.

CONCLUSION

A circulating 9-DEmiRNA set was significantly linked to both periodontitis and preeclampsia. Enrichment analysis identified specific genes, pathways, and functional mechanisms, which may be epigenetically altered and thereby mediate the biological association of periodontitis and preeclampsia.

摘要

目的

牙周病与包括子痫前期在内的妊娠并发症有关。本生物信息学研究旨在探讨循环 microRNA（miRNA）作为牙周病与子痫前期之间关联的中介物的可能作用。

方法

从基因表达综合数据库（GEO）中寻找牙周炎和对照组的外周血 miRNA 谱，并进行差异表达分析。从人类 microRNA 疾病数据库（HMDD v3.0）中确定与子痫前期相关的经过实验验证的循环 miRNA。绘制 Venn 图以识别共享的循环差异 miRNA（DEmiRNA）。使用 miRNA 富集分析和注释工具（miEAA v2.0）预测共享 DEmiRNA 的显著富集靶基因、KEGG 通路和基因本体论（GO）术语。此外，还分析了共享 DEmiRNA 富集靶基因在人类蛋白质组图谱中的富集 WikiPathways、BioCarta 代谢途径和组织蛋白。

结果

在牙周炎的 183 个循环 DEmiRNA 和子痫前期的 60 个经过实验验证的 miRNA 中，鉴定出 9 个共享的 DEmiRNA。在 32 个过表达靶基因中，前 3 位包括 MAFB、PSAP 和 CDK5RAP2；在 14 个富集的 KEGG 通路中，前 3 位是肾素-血管紧张素系统和移植物抗宿主病；在 44 个丰富的 GO 谱中，前 3 位包括“表皮生长因子激活受体活性的正调控”和“钙离⼦的螯合”。在过表达靶基因集中，在 10 个富集的 WikiPathways 中，前 3 位包括“NAD 代谢、沉默调节因子和衰老”和“小分子化合物对 Wnt/B-连环蛋白信号的调节”，PPAR 相关机制在 13 个富集的 BioCarta 代谢途径中居首位。

结论

一个循环的 9-DEmiRNA 集与牙周炎和子痫前期均显著相关。富集分析确定了特定的基因、通路和功能机制，这些基因、通路和功能机制可能发生表观遗传改变，从而介导牙周炎和子痫前期之间的生物学关联。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/771d/9293528/6c9733b52453/DM2022-2771492.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/771d/9293528/f4bf1ac1a6f1/DM2022-2771492.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/771d/9293528/13b775b6afaf/DM2022-2771492.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/771d/9293528/ca6e399ed8c6/DM2022-2771492.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/771d/9293528/42782ee34c5f/DM2022-2771492.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/771d/9293528/c9af79beac75/DM2022-2771492.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/771d/9293528/3d2545538175/DM2022-2771492.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/771d/9293528/6c9733b52453/DM2022-2771492.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/771d/9293528/f4bf1ac1a6f1/DM2022-2771492.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/771d/9293528/13b775b6afaf/DM2022-2771492.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/771d/9293528/ca6e399ed8c6/DM2022-2771492.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/771d/9293528/42782ee34c5f/DM2022-2771492.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/771d/9293528/c9af79beac75/DM2022-2771492.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/771d/9293528/3d2545538175/DM2022-2771492.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/771d/9293528/6c9733b52453/DM2022-2771492.007.jpg

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