Inhibition of Rgs10 aggravates periodontitis with collagen-induced arthritis via the nuclear factor-κB pathway.

Abstract

To explore the role of the Rgs10-associated nuclear factor (NF)-κB signalling pathway in periodontitis with rheumatoid arthritis. Porphyromonas gingivalis and collagen were locally applied to mice to establish in vivo periodontitis and rheumatoid arthritis models, respectively. Both agents were administered together to establish the comorbid group. All models were treated with adeno-associated virus-green fluorescent protein (AAV-GFP) or adeno-associated virus small hairpin Rgs10 (AAV-sh-Rgs10). In vivo expression of Rgs10 and inflammatory cytokines was analysed, along with exploration of the NF-κB signalling pathway in lipopolysaccharide-stimulated mouse-derived RAW264.7 cells, with and without treatment of small interfering RNA (siRNA; Rgs10-Mus-MSS245072). In the comorbidity mouse group (mice with both periodontitis and rheumatoid arthritis), inhibition of Rgs10 exacerbated periodontitis, along with upregulation of phospho-RelA (pP65), tumour necrosis factor-α (TNF-α) and interleukin-6 (IL-6) expression in the NF-κB signalling pathway. Similarly, treatment of LPS-stimulated RAW264.7 cells with siRNA resulted in the inhibition of Rgs10, along with upregulation of pP65, TNF-α and IL-6 expression in vitro. Inhibition of Rgs10 in mice with periodontitis and rheumatoid arthritis can promote the progression of periodontitis, indicating the potential therapeutic role of Rgs10 in this condition.