Inhibition of regulator of G protein signaling 10, aggravates rheumatoid arthritis progression by promoting NF-κB signaling pathway

Rheumatoid arthritis (RA) is the most common inflammatory arthropathy, with evidence pointing to an immune-mediated etiology that propagates chronic inflammation. Although targeted immune therapeutics and aggressive treatment strategies have substantially improved, a complete understanding of the associated pathological mechanisms of the disease remains elusive. This study aimed at investigating whether regulator of G protein signaling 10 (RGS10) could affect rheumatoid arthritis (RA) pathology by regulating the immune response. A DBA/J1 mouse model of RA was established and evaluated for disease severity. RGS10 expression was inhibited by adeno-associated virus in vivo. Moreover, small interfering RNA was used to downregulate RGS10 expression in raw 264.7 cells in vitro. Results showed that RGS10 inhibition augmented RA severity, and attenuated the increase in expression of inflammatory factors. Furthermore, activated NF-.B signaling pathways were detected following RGS10 inhibition. These results revealed that RGS10 inhibition directly aggravated the RA pathological process by activating the NF-kappa B signaling pathway. Therefore, RGS10 is a promising novel therapeutic target for RA treatment with a potential clinical impact.

Automated summary

This study found that inhibition of RGS10 directly aggravated the pathological process of rheumatoid arthritis by regulating immune response, and activated the NF-κB signaling pathway.