Mitochondrial abnormalities are involved in periodontal ligament fibroblast apoptosis induced by oxidative stress

Abstract

Oxidative stress (OS)-induced apoptosis of periodontal ligament cells (PDLCs) has been suggested to be an important pathogenic factor of periodontitis. Mitochondrial abnormalities are closely linked to OS and act as the main players in apoptosis. Our aim was to investigate the potential mitochondrial abnormalities in PDLCs apoptosis induced by OS. In this study, significant reduction in viability and increased apoptosis were observed in H₂O₂-treated hPDLCs. H₂O₂ also induced mitochondrial dysfunction, judging by increased mitochondrial reactive oxygen species amounts, and decreased mitochondrial membrane potential as well as ATP levels. Furthermore, H₂O₂ significantly enhanced mitochondrial fission by decreasing the expression of Mfn1 and Mfn2, along with increasing the expression of Drp1, Fis1 and the cleavage of OPA1. Notably, NAC stabilized the balance of the mitochondrial dynamics, attenuated mitochondrial dysfunction, and inhibited apoptosis of hPDLCs in the presence of H₂O₂. In conclusion, the OS-induced apoptosis of hPDLCs may be mediated by mitochondria-dependent pathway.

Keywords: Apoptosis; Human periodontal ligament cells; Mitochondrial abnormalities; Mitochondrial dynamics; Oxidative stress.