Dysregulated m6A methylation modification is associated with human peri-implantitis – A pilot study
N6-methyladenosine (m6A) RNA modification and its regulatory enzymes play important roles in the modulation of inflammation by regulating inflammation-related gene expression. Dysregulation of m6A has been associated with inflammatory diseases, including periodontitis. This study aimed to investigat...
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Published in | Journal of stomatology, oral and maxillofacial surgery Vol. 124; no. 6; p. 101550 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
France
01.12.2023
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Subjects | |
Online Access | Get full text |
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Summary: | N6-methyladenosine (m6A) RNA modification and its regulatory enzymes play important roles in the modulation of inflammation by regulating inflammation-related gene expression. Dysregulation of m6A has been associated with inflammatory diseases, including periodontitis. This study aimed to investigate the potential role of m6A modification and its master regulatory enzyme METTL3 in patients with peri‑implantitis.
Peri-implant soft tissues from 20 subjects (10 healthy controls and 10 patients with peri‑implantitis) were enrolled in this study. Quantitative reverse transcription PCR (RT-qPCR) was used to detect METTL3 gene expression and western blotting was used to detect METTL3 protein expression. The m6A mRNA levels were measured using an m6A-RNA methylation quantification kit. Protein-protein interaction networks and in silico functional analyses were conducted using various bioinformatics tools.
m6A mRNA levels significantly increased in the peri‑implantitis group. Higher METTL3 mRNA and protein levels were observed in the peri‑implantitis group. High METTL3 expression might influence elevated levels of m6A RNA methylation. In addition, in silico functional analysis indicated that the METTL3 gene and protein were associated with inflammatory pathways.
Our data provide evidence, for the first time, that dysregulation of m6A modification is associated with peri‑implantitis and may represent a strong risk factor for this inflammatory disease. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 2468-7855 2468-7855 |
DOI: | 10.1016/j.jormas.2023.101550 |