rheumatoid-arthritis
How does METTL3 fuel rheumatoid arthritis FLSs?
Open access · cc by · source: Europe PMC
METTL3 is upregulated in RA synovium and AIA rats; it boosts FLS inflammatory mediators and activation through NF-κB signalling.
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How does METTL3 fuel rheumatoid arthritis FLSs?
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RA synovial tissues from 5 patients (ages 40–70) were studied.
We received the synovial tissue from developing RA patients ( n = 5, aged 40–70 years) who were undergoing a synovectomy or joint replacement and who had been diagnosed on the basis of the rheumatology criteria revised by
OA control tissues came from 3 patients (ages 40–70).
Meanwhile, the control group involved osteoarthritis (OA) patients ( n = 3, aged 40–70 years).
Key findings
METTL3 was significantly upregulated in human RA synovium and the AIA model. Knockdown lowered IL-6, MMP-3, and MMP-9; overexpression raised them. Authors conclude METTL3 may promote FLS activation and inflammation via NF-κB.
Methodology
Compared METTL3 in RA vs OA synovial tissues, manipulated METTL3 in human RA-FLSs and rat AIA-FLSs, and probed inflammatory cytokines, MMPs, and NF-κB pathway activity.
Limitations
Small human tissue N (RA 5, OA 3) and mechanistic cell/animal work do not prove a clinical therapy; NF-κB is implicated but not a full patient trial.
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