Evidence map›Paper›PMID 40921962›Full record

ArticleIn vitro cellular & developmental biology. Animal2025

LncRNA TP53TG1 promotes the growth and osteo/dentinogenic differentiation of dental pulp stem cells by activating the Smad3 and JNK1/2 pathway.

Tingyue Li, Zihan Dai, Zhihua Wang, Minghao Wang, Chengxiong Cai, Xiaoru Zhu, Yang Zhao, Paul Roy Cooper, Shengchao Wang, Wenxi He

Abstract read
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In one paragraph

Article in In vitro cellular & developmental biology. Animal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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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

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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

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4 · The record

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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

10 authors.

Tingyue Li *Department of Stomatology, Air Force Medical Center, Air Force Medical University, 30 Fucheng Road, Beijing, 100142, PR China.
Zihan Dai *State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Key Laboratory of Stomatology, Department of Operative Dentistry and Endodontic, The Third Affiliated Hospital of Air Force Medical University, 145 Changle West Road, Xi'an, 710032, PR China.
Zhihua Wang *State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Key Laboratory of Stomatology, Department of Operative Dentistry and Endodontic, The Third Affiliated Hospital of Air Force Medical University, 145 Changle West Road, Xi'an, 710032, PR China.
Minghao WangState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Key Laboratory of Stomatology, Department of Operative Dentistry and Endodontic, The Third Affiliated Hospital of Air Force Medical University, 145 Changle West Road, Xi'an, 710032, PR China.
Chengxiong CaiDepartment of Stomatology, Air Force Medical Center, Air Force Medical University, 30 Fucheng Road, Beijing, 100142, PR China.
Xiaoru ZhuDepartment of Stomatology, Air Force Medical Center, Air Force Medical University, 30 Fucheng Road, Beijing, 100142, PR China.
Yang ZhaoDepartment of Stomatology, Air Force Medical Center, Air Force Medical University, 30 Fucheng Road, Beijing, 100142, PR China.
Paul Roy CooperDepartment of Oral Sciences, Sir John Walsh Research Institute, Faculty of Dentistry, University of Otago, PO Box 56, Dunedin, 9054, New Zealand.
Shengchao WangState Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, National Clinical Research Center for Oral Diseases, Shaanxi Key Laboratory of Stomatology, Department of Operative Dentistry and Endodontic, The Third Affiliated Hospital of Air Force Medical University, 145 Changle West Road, Xi'an, 710032, PR China. wangshengchao@fmmu.edu.cn.
Wenxi HeDepartment of Stomatology, Air Force Medical Center, Air Force Medical University, 30 Fucheng Road, Beijing, 100142, PR China. hewenxi7725@163.com.ORCID http://orcid.org/0000-0002-5353-0465

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TP53TG1 is a long non-coding RNA related to the TP53 gene, which plays an important role in various biological processes such as tumorigenesis, cell cycle regulation, and DNA damage repair. In recent years, researchers have begun to explore the role of TP53TG1 in dental pulp biology, especially its potential impact on pulpitis and other pulp-related diseases. However, the role of TP53TG1 in human dental pulp stem cells (hDPSCs) remains unclear. In this study, we obtained TP53TG1 knockdown dental pulp stem cells by plasmid transfection to determine the biological role of TP53TG1 in DPSCs. We found that the expression of TP53TG1 increased significantly during odontogenic differentiation of DPSCs. SiRNA knockdown of TP53TG1 expression resulted in inhibition of proliferation of hDPSCs. During odontogenic differentiation, downregulation of TP53TG inhibited the expression of multiple differentiation-related indices, and alkaline phosphatase activity and the formation of mineralized nodules were also inhibited. In addition, Western blot found that knockdown of TP53TG1 also weakened SMAD3 and JNK1/2 signaling in DPSCs. In conclusion, our study revealed the differentiation-inducing role of TP53TG1 in DPSCs, which plays an important role in dental pulp repair and regeneration and provides new insights and approaches for the prevention and treatment of dental pulp diseases.

Indexed as

Cell DifferentiationDental PulpDentinogenesisMAP Kinase Signaling SystemOsteogenesisRNA, Long NoncodingSmad3 ProteinStem CellsCell ProliferationGene Knockdown TechniquesHumansOdontogenesisRNA, Long NoncodingSmad3 ProteinSMAD3 protein, humanHDPSCsLncRNAOdontogenic differentiationProliferationTP53TG1

Identifiers

PMID40921962

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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.