Evidence map›Paper›PMID 39789287›Full record

ArticleInflammation2025

Dnmt3a-mediated DNA Methylation Regulates P. gingivalis-suppressed Cementoblast Mineralization Partially Via Mitochondria-dependent Apoptosis Pathway.

Heyu Liu, Li Ma, Huiyi Wang, Xin Huang, Yan Peng, Zhengkun Yang, Junhong Xiao, Hantao Huang, Qiudong Yang, Jiahui Sun and 4 more

Abstract read
In one paragraph

Article in Inflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors.

Heyu LiuState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, China.
Li MaState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, China.
Huiyi WangState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, China.
Xin HuangState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, China.
Yan PengState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, China.
Zhengkun YangState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, China.
Junhong XiaoState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, China.
Hantao HuangState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, China.
Qiudong YangState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, China.
Jiahui SunState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, China.
Xiaoxuan WangState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, China.
Chuan WangState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, China.
Liu YangState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, China.
Zhengguo CaoState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, China. caozhengguo@whu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDNA methyltransferase 3A (Dnmt3a) is an enzyme that catalyzes the de novo methylation of DNA, and plays essential roles in a wide range of physiological and pathological processes. However, it remains unclear whether Porphyromonas gingivalis affects cementoblasts, the cells responsible for cementum formation, through Dnmt3a.

methodsThe samples were collected from models of mouse periapical lesions and mice of different ages, and the expression of Dnmt3a was detected through immunofluorescence. Porphyromonas gingivalis was co-cultured with cementoblasts that simultaneously overexpressed Dnmt3a. Additionally, cementoblasts were subjected to either Dnmt3a knockout or DNA methylation inhibition. Changes in global DNA methylation were analyzed, and quantitative PCR, western blotting, alkaline phosphatase (ALP) activity assays, and Alizarin Red staining were employed to evaluate alterations in the mineralization capacity of cementoblasts.RNA sequencing further showed the mechanisms by which Dnmt3a regulated mineralization. Flow cytometry, MitoSox, and TRMR staining were used to verify the participation of mitochondria-dependent apoptosis.

resultsThe effect of P. gingivalis on Dnmt3a and global DNA methylation in cementoblasts was first verified. Dnmt3a expression and global DNA methylation were upregulated during cementoblast mineralization. Samples with periapical inflammation exhibited reduced Dnmt3a expression. P. gingivalis stimulation reduced the global DNA methylation and the mineralization ability of cementoblasts. Both the knockdown of Dnmt3a and using DNA methylation inhibitors suppressed cementoblast mineralization. In addition, Dnm3a depletion was significantly correlated with the mitochondria-dependent apoptosis pathway in cementoblasts.

conclusionsP. gingivalis blocks DNA methylation by silencing Dnmt3a in cementoblasts, thereby inducing mitochondrial-dependent apoptosis and, ultimately, impaired cementogenesis.

Indexed as

ApoptosisDental CementumDNA (Cytosine-5-)-MethyltransferasesDNA MethylationMitochondriaPorphyromonas gingivalisAnimalsDNA Methyltransferase 3AMiceDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3ADnmt3a protein, mouseApoptosisCell mineralizationCementumDNA methylationDNA methyltransferasePorphyromonas gingivalis

Identifiers

PMID39789287
PMCPMC12596322

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.