Evidence map›Paper›PMID 39713307›Full record

ArticlebioRxiv : the preprint server for biology2025

CRISPR-Edited DPSCs, Constitutively Expressing BDNF Enhance Dentin Regeneration in Injured Teeth.

Ji Hyun Kim, Muhammad Irfan, Sreelekshmi Sreekumar, Atsawasuwan Phimon, Seung Chung

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

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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

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors.

Ji Hyun KimDepartment of Oral Biology, College of Dentistry, University of Illinois Chicago, Chicago 60612, IL, USA.
Muhammad IrfanDepartment of Oral Biology, College of Dentistry, University of Illinois Chicago, Chicago 60612, IL, USA.
Sreelekshmi SreekumarDepartment of Oral Biology, College of Dentistry, University of Illinois Chicago, Chicago 60612, IL, USA.
Atsawasuwan PhimonDepartment of Oral Biology, College of Dentistry, University of Illinois Chicago, Chicago 60612, IL, USA.
Seung ChungDepartment of Oral Biology, College of Dentistry, University of Illinois Chicago, Chicago 60612, IL, USA.ORCID 0000-0003-1449-8762

Funding

Role of complement receptor C5L2 in reparative dentinogenesisR01DE029816 · NIDCR · UNIVERSITY OF ILLINOIS AT CHICAGO · PI CHUNG, SEUNG · 2022 to 2025
$1.9M
Role of complement receptor C5L2 in reparative dentinogenesisR56DE029816 · NIDCR · UNIVERSITY OF ILLINOIS AT CHICAGO · PI CHUNG, SEUNG · 2020 to 2020
$380k
NIDCR NIH HHS R01 DE029816NIDCR NIH HHS R56 DE029816
6 · The paper itself

Abstract

Dental caries, a prevalent global health issue, results from complex bacterial interactions. In response to harmful stimuli, a desirable outcome for the tooth is the formation of tertiary dentin, a protective reparative process that generates new hard tissue. This reparative dentinogenesis is associated with significant inflammation, which triggers the recruitment and differentiation of dental pulp stem cells (DPSCs). Previously, we have demonstrated that brain-derived neurotrophic factor (BDNF) and its receptor TrkB, key mediators of neural functions, are activated during the DPSC-mediated dentin regeneration process. In this study, we further define the role of inflammation in this process and apply stem cell engineering to enhance dentin regeneration in injured teeth. Our data show that TrkB expression and activation in DPSCs rapidly increase during odontogenic differentiation, further amplified by inflammatory inducers and mediators such as TNFα, LTA, and LPS. An in vivo dentin formation assessment was conducted using a mouse pulp-capping/caries model, where CRISPR-engineered DPSCs overexpressing BDNF were transplanted into inflamed pulp tissue. This transplantation significantly enhanced dentin regeneration in injured teeth. To further explore potential downstream pathways, we conducted transcriptomic profiling of TNFα-treated DPSCs, both with and without TrkB antagonist CTX-B. The results revealed significant changes in gene expression related to immune response, cytokine signaling, and extracellular matrix interactions. Taken together, our study advances our understanding of the role of BDNF in dental tissue engineering using DPSCs and identifies potential therapeutic avenues for improving dental tissue repair and regeneration strategies.

Indexed as

BDNFDental cariesDentinogenesisRegenerationTNFαTrKB

Identifiers

PMID39713307
PMCPMC11661210

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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.