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

AI Article Synopsis

  • Dental caries is a widespread health issue linked to bacteria, prompting the tooth to form protective tertiary dentin, facilitated by inflammation and dental pulp stem cells (DPSCs).
  • The research investigates how inflammation boosts TrkB expression in DPSCs, highlighting its importance in dentin regeneration, particularly when enhanced through CRISPR-engineered DPSCs that overexpress brain-derived neurotrophic factor (BDNF).
  • Results from a mouse model demonstrate that BDNF-engineered DPSCs significantly improve dentin regeneration, with transcriptomic analysis revealing crucial changes in genes related to immune response and tissue repair pathways.

Article Abstract

Dental caries is one of the most common health issues worldwide arising from the complex interactions of bacteria. In response to harmful stimuli, 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 shown 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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11661210PMC
http://dx.doi.org/10.1101/2024.12.11.627879DOI Listing

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