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

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 (PDLSCs) and provide a new strategy for treatment or prevention of periodontitis.

Methods: We used immunohistochemistry to detect the LC3 expression in periodontal ligament (PDL) tissues from patients with (n = 20) or without (n = 20) periodontitis. To further investigate the mechanism of autophagy, the PDLSCs were divided into three groups: H-PDLSCs, P-PDLSCs and I-PDLSCs. The level of autophagy in PDLSCs was evaluated by qRT-PCR and Western blot. LC3-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 LC3, Beclin-1, Atg7 and Atg12 in P-PDLSCs and I-PDLSCs. We also detected LC3-positive points and AVs in P-PDLSCs and I-PDLSCs. The activation of autophagy may protect PDLSCs from apoptosis.

Conclusion: The results indicate that the modulation of autophagy in P-PDLSCs may provide a novel therapeutic strategy to improve periodontal therapy.

Keywords: TNF-α; autophagy; inflammation; periodontal ligament stem cells.