Epigenetic Regulatory Axis MIR22‐TET3‐MTRNR2L2 Represses Fibroblast‐Like Synoviocyte–Mediated Inflammation in Rheumatoid Arthritis
Authors' conclusion
The key role of the MIR22-TET3-MTRNR2L2 pathway in RA-FLSs provided an experimental basis for further studies into the pathogenesis and related targets of RA from the perspective of FLSs.
Study context
- Population
- Synovium of patients with rheumatoid arthritis (RA) and arthritic mice; RA-FLSs
Methodological detailsMir22-/- and Tet3+/- mice collagen antibody-induced arthritis (CAIA) model, CIA model, in vitro RA-FLS experiments
- Mir22-/- and Tet3+/- mice CAIA model
- CIA model
- In vitro RA-FLS experiments
Main finding
As reported in the abstract
- MIR22 inhibited inflammation (Mir22-/- CAIA model and RA-FLS in vitro experiments)
- MIR22 directly inhibits translation of TET3 in RA-FLSs by binding its 3' untranslated region
- Tet3+/- CAIA mice showed less severe arthritis in vivo; in vitro experiments confirmed proinflammatory effect of TET3 in RA
- Therapeutic effects of Mir22 angomir and Tet3 small interfering RNA (siRNA) validated in CIA model
- TET3 exerts its proinflammatory effect by promoting 5hmC production in the promoter of its target MTRNR2L2 in RA-FLSs
Original publication
Epigenetic Regulatory Axis MIR22‐TET3‐MTRNR2L2 Represses Fibroblast‐Like Synoviocyte–Mediated Inflammation in Rheumatoid Arthritis. Arthritis Rheumatol. Published 7 March 2024. doi:10.
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