METTL14‐Mediated Methyladenosine (m6A) Modification of TNFAIP3 Involved in Inflammation in Patients With Active Rheumatoid Arthritis
Authors' conclusion
Our study highlights the critical roles of m6A on regulation of inflammation in RA progression.
Study context
- Population
- Peripheral blood mononuclear cells (PBMCs) from patients with rheumatoid arthritis (RA) and healthy controls; Collagen antibody-induced arthritis (CAIA) mice
- Comparison
- Patients with RA vs healthy controls; METTL14 knockdown
- Outcome
- Role of m6A modification in the progression of RA
Methodological detailsin vitro PBMC studies, in vivo CAIA mouse model
- In vitro PBMC studies
- In vivo CAIA mouse model
Main finding
As reported in the abstract
- METTL14 and m6A levels decreased in PBMCs of patients with active RA and correlated negatively with DAS28
- METTL14 knockdown downregulated m6A and promoted secretion of IL-6 and IL-17 in PBMCs of patients with RA
- METTL14 knockdown promoted joint inflammation with upregulation of IL-6 and IL-17 in CAIA mice
- TNFAIP3, a key suppressor of the NF-κB inflammatory pathway, was involved in m6A-regulated PBMCs
- m6A affected TNFAIP3 expression by regulating mRNA stability and translocation in TNFAIP3 protein coding sequence
Original publication
METTL14‐Mediated m6A Modification of TNFAIP3 Involved in Inflammation in Patients With Active Rheumatoid Arthritis. Arthritis Rheumatol. Published 28 September 2023. doi:10.
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