Background/Purpose We previously reported that adiponectin (AD) is highly expressed in the inflammatory joint of rheumatoid arthritis (RA) patients and closely correlated with progressive bone erosion, but the mechanism remained largely unclear. Synovial fibroblasts from RA patients (RASFs) have been suggested a unique characteristic of resistance to apoptosis that contributes to synovial hyerplasia, synovitis and bone erosion in RA. In this study, we tested the role of AD on apoptosis and proliferation in primary RASFs.

Methods RASFs was treated with PBS in the absence and presence of AD (0.1, 1 or 10 μg/ml) for 24 h to 72 h and the frequencies of apoptosis cells were measured by flow cytometry. CCK-8 and direct microscopic count were used to analyze the proliferation of RASFs after stimulated with AD. Real-time PCR was used to test the expression of Bcl-2, Bax, p53, CDK4, PCNA, IL-6, IL-8 and MMP-3 mRNA in RASFs. Western blot was used to test the protein expression of Bcl-2 and Bax and activation of signal transduction pathways.

Results The frequencies of apoptosis cells were significant decreased in RASFs after AD stimulation. AD could promote proliferation of RASFs compared with untreated it. A markedly increased CDK4 and PCNA mRNA expression and a decreased level of p53 mRNA were observed in RASFs after treated with AD. The levels of IL-6, IL-8 and MMP-3 expression also obviously increased in RASFs upon AD stimulation. Western blot indicated that AD could rapidly triggered p-Akt and p-ERK activity and then induced Bcl-2, but decreased Bax expression in RASFs.

Conclusion Our findings indicate that AD could affect apoptosis and proliferation of RASFs via Akt and ERK pathway, suggesting a critical role of AD on disease progression in RA.

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ACR Meeting Abstracts - https://acrabstracts.org/abstract/modulatory-effect-of-adiponectin-on-apoptosis-and-proliferation-of-synovial-fibroblasts-from-rheumatoid-arthritis-patients/