KDM2B and its peptides promote the stem cells from apical papilla mediated nerve injury repair in rats by intervening EZH2 function

Cell Proliferation, 2025 · DOI: 10.1111/cpr.13756 · Published: March 1, 2025

Simple Explanation

This study explores how a protein called KDM2B affects nerve regeneration using stem cells from dental apical papilla (SCAP). It found that KDM2B enhances the ability of these stem cells to become nerve cells. The research also showed that KDM2B interacts with another protein, EZH2, which normally suppresses nerve cell development. By using specific protein sequences (peptides) from KDM2B, the researchers were able to block EZH2's function, further promoting nerve regeneration. In rats with spinal cord injuries, transplanting SCAP treated with these KDM2B peptides led to improved motor function recovery, suggesting a potential new approach for nerve injury treatment.

Study Duration

4 Weeks

Participants

32 Sprague–Dawley rats

Evidence Level

Not specified

Key Findings

1
KDM2B promotes neurogenic differentiation in SCAP cells by enhancing the expression of neurogenic markers and neural sphere formation.
2
KDM2B negatively regulates EZH2, a protein that suppresses neurogenic ability, and their interaction decreases during neurogenic differentiation.
3
KDM2B-derived peptides can effectively intervene with EZH2 function, promoting neurogenic differentiation of SCAP cells and improving functional recovery in spinal cord injury rat models.

Research Summary

This study investigates the role of KDM2B in promoting neurogenic differentiation of mesenchymal stem cells (MSCs) from dental apical papilla (SCAP) and its impact on nerve injury repair in rats. The research demonstrates that KDM2B enhances neurogenic indicators, modifies H3K4me3 methylation on neurogenesis-related genes, and improves motor ability recovery in spinal cord injury (SCI) rats at the early healing stage. Furthermore, the study identifies key protein binding sequences between KDM2B and EZH2, and shows that KDM2B-peptides can intervene with EZH2 function to promote SCAP-mediated functional recovery at the SCI early phase.

Practical Implications

Therapeutic Potential

KDM2B-peptides could be developed as candidate agents for enhancing the neurogenic ability of MSCs and improving nerve injury repair.

Epigenetic Targets

The study highlights the importance of epigenetic modifications, specifically H3K4me3, in regulating neurogenesis and provides insights into potential therapeutic targets.

Drug Development

The identified key protein interaction sites between KDM2B and EZH2 can be targeted for developing drugs that promote nerve regeneration.

Study Limitations

1
Further research is needed to optimize the usage concentration and treatment time of KDM2B-peptides.
2
The study primarily focuses on the early phase of spinal cord injury; long-term effects need to be investigated.
3
The study is conducted on rats; translation to human clinical trials requires further validation.

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