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Synoviolin is not a pathogenic factor for auto-inflammatory diseases.
- Source :
-
Biochemical & Biophysical Research Communications . Jun2021, Vol. 558, p183-188. 6p. - Publication Year :
- 2021
-
Abstract
- 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. • Synoviolin is a pathogenic factor for rheumatoid arthritis, an auto-immune diseases. •Synoviolin accumulates in synovial cells of joints in hIL-1 cTg mouse, an auto-inflammatory disease model. •Arthritis and joint destruction seen in hIL-1 cTg mice are unchanged by Synoviolin deficiency. •Synoviolin dose not promote auto-inflammatory disease development. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 0006291X
- Volume :
- 558
- Database :
- Academic Search Index
- Journal :
- Biochemical & Biophysical Research Communications
- Publication Type :
- Academic Journal
- Accession number :
- 150207291
- Full Text :
- https://doi.org/10.1016/j.bbrc.2021.04.093