Thioredoxin-1 promotes the restoration of alveolar bone in periodontitis with diabetes
Treatment of periodontitis in people with diabetes remains challenging. Diabetes-enhanced oxidative stress is a primary cause of aggravation of periodontitis. The present study aimed to investigate the therapeutic potential of thioredoxin-1 (TRX1), an essential endogenous antioxidant protein, in the management of periodontitis with diabetes, as well as its role in modulating osteogenic differentiation. Our findings indicated that the production of reactive oxygen species (ROS) was elevated, while the expression of TRX1 was significantly reduced in the periodontal tissues of periodontitis mice with diabetes. Furthermore, knockdown of TRX1 in periodontal ligament stem cells (PDLSCs) resulted in the inhibition of osteogenic differentiation through disrupting Wnt/ß-catenin signal pathway. However, this inhibition was restored upon administration of recombinant human TRX1 (rhTRX1). Importantly, rhTRX1 treatment decreased ROS generation, activated Wnt/ß-catenin signal pathway and considerably promoted the alveolar bone repair of periodontitis mice with diabetes. These findings highlighted the crucial protective role of TRX1 in periodontitis with diabetes and suggested that it may serve as a potential therapeutic target for refractory periodontitis associated with oxidative stress. Overall design: To explore the mechanism underlying the regulatory function of thioredoxin (TRX1) in osteogenic differentiation, we used LV-sh-TRX1 vector to transfact human periodontal ligament sten cells (PDLSCs) to knock down the TRX1 expression. We then performed RNA sequencing comparing TRX1 knockdown PDLSCs and normal PDLSCs under osteogenic induction. The differentially expressed genes (DEG) were further analysed.