Increased autophagy is required to protect periodontal ligament stem cells from apoptosis in inflammatory microenvironment

Abstract

Abstract Objective Autophagy, which provides a mechanism for turnover cellular organelles and proteins through a lysosome‐dependent degradation pathway, has been related to the pathogenesis of inflammatory disorders and other diseases. Therefore, the aim of this research was to study the role of autophagy in periodontal ligament stem cells ( PDLSC s) and provide a new strategy for treatment or prevention of periodontitis. Methods We used immunohistochemistry to detect the LC 3 expression in periodontal ligament ( PDL ) tissues from patients with (n = 20) or without (n = 20) periodontitis. To further investigate the mechanism of autophagy, the PDLSC s were divided into three groups: H‐ PDLSC s, P‐ PDLSC s and I‐ PDLSC s. The level of autophagy in PDLSC s was evaluated by qRT ‐ PCR and Western blot. LC 3‐positive points were assessed by immunofluorescence, and the autophagic vacuoles (AVs) were observed by transmission electron microscope. Results We found a higher level of autophagy in gene expression and autophagosome production of PDL tissues from periodontitis patients. Furthermore, there were higher protein levels of LC 3, Beclin‐1, Atg7 and Atg12 in P‐ PDLSC s and I‐ PDLSC s. We also detected LC 3‐positive points and AVs in P‐ PDLSC s and I‐ PDLSC s. The activation of autophagy may protect PDLSC s from apoptosis. Conclusion The results indicate that the modulation of autophagy in P‐ PDLSC s may provide a novel therapeutic strategy to improve periodontal therapy.