RNA-binding protein Lin28 is associated with injured dentin-dental pulp complex in Sprague-Dawley rats.

Reactivation of Lin28 accelerates hair, cartilage, bone and mesenchyme regrowth after ear and digit injuries. However, the relationship of Lin28 to reparative dentin has been under investigation. The aim of the present study was to examine whether Lin28 participates in the reparative dentin process and lipopolysaccharide (LPS)-stimulated human dental pulp cells (HDPCs) and to identify the underlying signaling pathway mechanisms. The study established a wound-healing model of the dentin-dental pulp complex in vivo and LPS-induced dental pulp cell inflammation in vitro. In vivo, the results of hematoxylin and eosin staining demonstrated the obvious appearance of reparative dentin and odontoblast-like cells were arranged along the reparative dentin. Immunohistochemical examination demonstrated that Lin28 expression was increased by 72 h after cavity preparation but was decreased by 21 d after cavity preparation. In vitro, HDPCs were exposed to 100 ng/ml LPS for 24 h, and the expression of Lin28 was increased. Overexpression of Lin28 was associated with the downregulated expression of let-7b, let-7g and miR-98. These findings suggest that the wound-healing model was successfully established. Lin28 was involved in the reparative process of the dentin-dental pulp complex and HDPCs exposed to LPS, and Lin28/let-7 may be the underlying mechanism.