BDNF/TrkB Is a Crucial Regulator in the Inflammation-Mediated Odontoblastic Differentiation of Dental Pulp Stem Cells

The odontoblastic differentiation of dental pulp stem cells (DPSCs) associated with caries injury happens in an inflammatory context. We recently demonstrated that there is a link between inflammation and tissue regeneration, identified via enhanced DPSC-mediated dentinogenesis vitro. Brain-derived neurotrophic factor (BDNF) nerve growth factor-related gene family molecule which functions through tropomyosin receptor kinase B (TrkB). While the roles BDNF neural repair other regeneration processes are well identified, its role has not been explored. Furthermore, receptor-TrkB inflammation-induced remains unknown. BDNF/TrkB was examined during 17-day odontogenic DPSCs. Human DPSCs were subjected to dentinogenic media treated inducers (LTA or TNFα), BDNF, TrkB agonist (LM22A-4) and/or antagonist (CTX-B). Our data show receptors affect early late stages Immunofluorescent confirmed expression ELISA qPCR demonstrate treatment increased dentin matrix protein-1 (DMP-1) DPSC differentiation. Coherently, levels runt-related transcription 2 (RUNX-2) osteocalcin (OCN) increased. TNFα, responsible for diverse range signaling, sialophosphoprotein (DSPP) DMP1. significantly potentiated effect. application CTX-B reversed this effect, suggesting TrkB`s critical TNFα-mediated dentinogenesis. studies provide novel findings on BDNF-TrkB This finding will address regulatory pathway therapeutic approach engineering using