RGS10 negatively regulates apical periodontitis via TFEB‐mediated autophagy in BABL/c mice model and in vitro

AIM: Apical periodontitis is a prevalent oral inflammatory disease that has recently been linked to transcription factor EB (TFEB)-mediated autophagy. Regulator of G-protein signalling 10 (RGS10) is reported to be an effective regulator of the immune system and inflammation. This study aimed to investigate the involvement of RGS10 during the development of apical periodontitis through the TFEB-mediated autophagy signalling pathway. METHODOLOGY: Sixty BALB/c mice were randomly divided into four groups of 15 mice for the in vivo experiment. Rgs10 was locally overexpressed through eight injections of an adeno-associated virus vector. The model of apical periodontitis was established 21 days following pulp exposure, and the mice were euthanized to obtain mandibles for analysis. Micro-computed tomography was employed to assess alveolar bone destruction, and the levels of Rgs10, TFEB-mediated autophagy signalling factors and inflammatory factors were measured using quantitative reverse transcription polymerase chain reactions, western blotting, enzyme-linked immunosorbent assays, immunofluorescence and immunohistochemistry. All experimental results were displayed as images or graphs. For the in vitro experiments, we employed small interfering RNA (siRNA) to silence Rgs10 expression in RAW 264.7 cells. The data were analysed via one-way anova or Mann-Whitney U test/Kruskal-Wallis test of variance, where p < .05 or U > 1.96 was considered statistically significant. RESULTS: Local overexpression of Rgs10 reduced alveolar bone destruction within the apical periodontitis lesion and significantly decreased macrophage infiltration (p < .05). Meanwhile, the expression of TFEB-mediated autophagy signalling factors was upregulated, along with a decrease in inflammatory factor expression (p < .05). Lipopolysaccharide-stimulated RAW 264.7 cells exhibited decreased Rgs10 expression and TFEB-mediated autophagy signalling. siRNA-mediated silencing of Rgs10 further suppressed autophagy and concomitantly upregulated inflammatory factors (p < .05). CONCLUSIONS: Collectively, the findings revealed that RGS10 suppresses the inflammatory response and bone destruction through TFEB-mediated autophagy in apical periodontitis.