Evidence map›Paper›PMID 42384314›Full record

ArticleTissue engineering and regenerative medicine2026

In-Depth Analysis of AG73-Dental Pulp Cell Interactions Underlying Adhesion and Mineralization: Insights from Alanine Scanning.

Jia Tang, Akimi Muramatsu, Youjing Qiu

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Article in Tissue engineering and regenerative medicine, 2026. 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

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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Jia TangShanghai Engineering Research Center for Tooth Restoration and Regeneration, School of Stomatology, Tongji University, Shanghai, 200072, People's Republic of China. mathlover2004@163.com.ORCID http://orcid.org/0000-0002-5025-2674
Akimi MuramatsuShanghai Engineering Research Center for Tooth Restoration and Regeneration, School of Stomatology, Tongji University, Shanghai, 200072, People's Republic of China.
Youjing QiuStomatological Hospital of Xiamen Medical College & Xiamen Key Laboratory of Stomatological Disease Diagnosis and Treatment, Xiamen, 361008, People's Republic of China.

Funding

National Natural Science Foundation of China 82301037
6 · The paper itself

Abstract

backgroundThis study aimed to explore the dental applications of AG73, a laminin-derived adhesive peptide, by examining its effects on human dental pulp cells (hDPCs), particularly in cell adhesion and mineralization. It also sought to identify the key functional residue of AG73 and the signaling pathways involved in its pro-mineralization activity.

methodsWe compared AG73's pro-mineralization activity with peptides derived from LAMA5 using alizarin red staining. Immunofluorescence staining assessed its cell adhesion properties. Alanine-scanning mutagenesis was performed to identify key residues for AG73's adhesion activity. Finally, we used p38 and JNK MAPK inhibitors to determine which signaling pathways were involved in AG73-induced mineralization.

resultsAG73 exhibited superior pro-mineralization activity compared to other peptides derived from LAMA5 in hDPCs. Immunofluorescence staining confirmed AG73's strong cell adhesive ability within 20 minutes. Alanine-scanning identified isoleucine at the tenth position as crucial for adhesion. AG73 was the most effective peptide in inducing mineralization, with no mutated versions outperforming it. p38 signaling was found to play a positive role in AG73-induced mineralization, while JNK inhibition enhanced mineralization, suggesting JNK inhibitors as potential inducers.

conclusionAG73 has strong pro-mineralization activity and significant cell adhesive properties in hDPCs. The isoleucine at the tenth amino acid position was identified as a critical residue for AG73's adhesive ability. Additionally, p38 was found to be involved in AG73-regulated mineralization, while JNK inhibition promoted the process. This is the first study to explore AG73's effects in hDPCs and provides a foundation for its potential use as a dental-pulp regenerative material.

Indexed as

AlanineCalcification, PhysiologicCell CommunicationDental PulpLamininPeptidesAmino Acid SequenceCell AdhesionDental Enamel ProteinsHumansJNK Mitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesAlanineAMBN protein, humanDental Enamel ProteinsJNK Mitogen-Activated Protein KinasesLamininp38 Mitogen-Activated Protein KinasesPeptidesCell adhesionCell adhesive peptideDental pulp cellsMineralization

Identifiers

PMID42384314
PMCPMC13415405

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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.