Exosome‑derived lncRNA‑Ankrd26 promotes dental pulp restoration by regulating miR‑150‑TLR4 signaling.

Abstract

At present, retaining the biological function of dental pulp is an urgent requirement in the treatment of pulp disease; it has been recognized that application of dental pulp stem cells (DPSCs) in regenerating dental pulp and dentin complexes is expected to become a safe and effective treatment of pulp disease; meanwhile the role of DPSC‑derived exosomes in dental pulp regeneration and repair is gaining attention. However, the underlying mechanism of DPSCs in dental pulp regeneration and repair is still unclear. In the present study, a variety of invitro biological experiments and an animal model, as well as next‑generation sequencing and bioinformatics analysis, demonstrated that DPSCs promoted migration and osteoblastic differentiation of mesenchymal stem cells (MSCs) via exosomes; this was induced by DPSC‑derived exosomal long non‑coding (lnc)RNA‑ankyrin repeat domain (Ankrd)26. Mechanistically, the effect of exosomal lncRNA‑Ankrd26 on migration and osteoblastic differentiation of MSCs was dependent on microRNA (miR)‑150/Toll‑like receptor (TLR)4 signaling; this was regulated by lncRNA‑Ankrd26. The present study demonstrated that exosomes‑derived lncRNA‑Ankrd26 from DPSCs promoted dental pulp restoration via regulating miR‑150‑TLR4 signaling in MSCs; these findings help to understand the mechanism of dental pulp repair, identify therapeutic targets in the development of pulpitis and develop clinical treatments.