Evidence map›Paper›PMID 38556862›Full record

ArticleBMC oral health2024

KAT2A-mediated succinylation modification of notch1 promotes the proliferation and differentiation of dental pulp stem cells by activating notch pathway.

Longwei Ye, Zeqin Yu, Lin He, Jie Yuan, Xiaodan Zhang, Lei Li, Xin Huang, Yanyan Ma, Lei Zhang

Open access · goldAbstract read
In one paragraph

Article in BMC oral health, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
5.3field-weighted citation impact, top 4% of its field
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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.

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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

9 authors at 3 institutions in 1 country.

Longwei Ye *Department of Oral Health and Prevention, The First Affiliated Hospital of Harbin Medical University. Harbin Medical University, School of Stomatology, No.143 Yiman Street, Nangang District, Harbin City, 150001, Heilongjiang Province, China.
Zeqin Yu *Department of Oral Health and Prevention, The First Affiliated Hospital of Harbin Medical University. Harbin Medical University, School of Stomatology, No.143 Yiman Street, Nangang District, Harbin City, 150001, Heilongjiang Province, China.
Lin HeDepartment of Stomatology, Heilongjiang Province Hospital, Harbin City, 150081, Heilongjiang Province, China.
Jie YuanDepartment of Oral Health and Prevention, The First Affiliated Hospital of Harbin Medical University. Harbin Medical University, School of Stomatology, No.143 Yiman Street, Nangang District, Harbin City, 150001, Heilongjiang Province, China.
Xiaodan ZhangDepartment of Oral Health and Prevention, The First Affiliated Hospital of Harbin Medical University. Harbin Medical University, School of Stomatology, No.143 Yiman Street, Nangang District, Harbin City, 150001, Heilongjiang Province, China.
Lei LiDepartment of Oral Health and Prevention, The First Affiliated Hospital of Harbin Medical University. Harbin Medical University, School of Stomatology, No.143 Yiman Street, Nangang District, Harbin City, 150001, Heilongjiang Province, China.
Xin HuangDepartment of Oral Health and Prevention, The First Affiliated Hospital of Harbin Medical University. Harbin Medical University, School of Stomatology, No.143 Yiman Street, Nangang District, Harbin City, 150001, Heilongjiang Province, China.
Yanyan MaPharmaceutical Department, The First Affiliated Hospital of Harbin Medical University, Harbin City, 150001, Heilongjiang Province, China.
Lei ZhangDepartment of Oral Health and Prevention, The First Affiliated Hospital of Harbin Medical University. Harbin Medical University, School of Stomatology, No.143 Yiman Street, Nangang District, Harbin City, 150001, Heilongjiang Province, China. 600985@hrbmu.edu.cn.
Harbin Medical University · CNFirst Affiliated Hospital of Harbin Medical University · CNHeilongjiang Provincial Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDental pulp stem cells (DPSCs) are a kind of undifferentiated dental mesenchymal stem cells with strong self-renewal ability and multi-differentiation potential. This study aimed to investigate the regulatory functions of succinylation modification in DPSCs.

methodsDPSCs were isolated from the dental pulp collected from healthy subjects, and then stem cell surface markers were identified using flow cytometry. The osteogenic differentiation ability of DPSCs was verified by alkaline phosphatase (ALP) and alizarin red staining methods, while adipogenic differentiation was detected by oil red O staining. Meanwhile, the mRNA of two desuccinylases (SIRT5 and SIRT7) and three succinylases (KAT2A, KAT3B, and CPT1A) in DPSCs before and after mineralization induction were detected using quantitative real-time PCR. The cell cycle was measured by flow cytometry, and the expression of bone-specific genes, including COL1a1 and Runx2 were evaluated by western blotting and were combined for the proliferation and differentiation of DPSCs. Co-immunoprecipitation (co-IP) and immunofluorescence were combined to verify the binding relationship between proteins.

resultsThe specific markers of mesenchymal stem cells were highly expressed in DPSCs, while the osteogenic differentiation ability of isolated DPSCs was confirmed via ALP and alizarin red staining. Similarly, the oil red O staining also verified the adipogenic differentiation ability of DPSCs. The levels of KAT2A were found to be significantly upregulated in mineralization induction, which significantly decreased the ratio of G0/G1 phase and increased S phase cells; converse results regarding cell cycle distribution were obtained when KAT2A was inhibited. Moreover, overexpression of KAT2A promoted the differentiation of DPSCs, while its inhibition exerted the opposite effect. The elevated KAT2A was found to activate the Notch1 signaling pathway, which succinylated Notch1 at the K2177 site to increase their corresponding protein levels in DPSCs. The co-IP results showed that KAT2A and Notch1 were endogenously bound to each other, while inhibition of Notch1 reversed the effects of KAT2A overexpression on the DPSCs proliferation and differentiation.

conclusionKAT2A interacted directly with Notch1, succinylating the Notch1 at the K2177 site to increase their corresponding protein levels in DPSCs. Similarly, KAT2A-mediated succinylation modification of Notch1 promotes the DPSCs proliferation and differentiation, suggesting that targeting KAT2A and Notch1 may contribute to tooth regeneration.

Indexed as

AnthraquinonesAzo CompoundsOsteogenesisStem CellsCell DifferentiationCell ProliferationCells, CulturedDental PulpHistone AcetyltransferasesHumansp300-CBP-Associated FactoralizarinAnthraquinonesAzo CompoundsHistone AcetyltransferasesKAT2A protein, humanoil red Op300-CBP-Associated FactorDental pulp stem cellsKAT2ANotch1Osteogenic differentiationSuccinylation

Identifiers

PMID38556862
PMCPMC10981825
OpenAlexW4393355470

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.