| First Author | Matsumoto T | Year | 2021 |
| Journal | Biochem Biophys Res Commun | Volume | 558 |
| Pages | 183-188 | PubMed ID | 33932778 |
| Mgi Jnum | J:305609 | Mgi Id | MGI:6706073 |
| Doi | 10.1016/j.bbrc.2021.04.093 | Citation | Matsumoto T, et al. (2021) Synoviolin is not a pathogenic factor for auto-inflammatory diseases. Biochem Biophys Res Commun 558:183-188 |
| abstractText | Auto-inflammatory syndromes are rare diseases characterized by arthritis and joint destruction, symptoms similar to but distinct from rheumatoid arthritis (RA). Therapeutic targets have not been well characterized for auto-inflammatory syndromes, although the E3 ligase Synoviolin was previously shown to be a novel therapeutic target for RA. Here, we show that Synoviolin loss has little impact on a model of auto-inflammatory diseases. We previously established such a model, the hIL-1 cTg mouse, in which IL-1 signaling was constitutively activated, and animals exhibit symptoms recapitulating auto-inflammatory syndromes such as major joint dominant arthritis. Here, we crossed hIL-1 cTg with Synoviolin flox'd mice to yield hIL-1 cTg/Synoviolin cKO mice. Synoviolin gene expression was ablated in adult hIL-1 cTg/Synoviolin cKO mice by injection of pIpC to activate Mx1 promoter-driven Cre recombinase. However, symptoms seen in hIL-1 cTg mice such as arthritis and joint destruction were not alleviated by targeting Synoviolin, ruling out Synoviolin as a therapeutic target for auto-inflammatory disease. Our results indicate that although similar, RA and auto-inflammatory diseases are different diseases, and treatment strategies should differ accordingly. |
