TTC4 inhibits NLRP3 inflammation in rheumatoid arthritis by HSP70.

OBJECTIVE

This experiment explored the function of TTC4 in rheumatoid arthritis inflammation and its possible mechanism.

METHODS

C57BL/6 mice were immunized intradermally with bovine type II collagen. Lipopolysaccharide induction was performed on RAW264.7 cells.

RESULTS

The mRNA expression of TTC4 in articular tissue of mice with rheumatoid arthritis was downregulated. Sh-TTC4 virus increased arthritis score, morphological change score, paw edema, and spleen index, as well as alkaline phosphatase level in mice with rheumatoid arthritis. Sh-TTC4 virus increased the levels of inflammatory factors and MDA, and decreased anti-oxidant factors in articular tissue of mice with rheumatoid arthritis. TTC4 reduced inflammation and oxidative stress in an in vitro model. TTC4 regulated HSP70 in a rheumatoid arthritis model. The inhibition of HSP70 reduced the effects of sh-TTC4 gene in mice with rheumatoid arthritis. METTL3 reduced the stability of the TTC4 gene.

CONCLUSION

In this study, the TTC4 gene reduced oxidative response and inflammation in the rheumatoid arthritis model through the HSP70/NLRP3 pathway. Therefore, it can be concluded that TTC4 can be used as diagnosis and prognosis evaluation of rheumatoid arthritis.