Peroxiredoxin-4 (PRDX4), a member of PRDX family, which played an important role in scavenging reactive oxygen species (ROS). The up-regulation of PRDX4 in synovial tissue and synovial fluid from rheumatoid arthritis (RA) patients has been reported. However, the biological functions of PRDX4 in fibroblast-like synoviocytes (RA-FLS) remains unclear. In this research, we reveal that expression of PRDX4 was notably increased in RA synovial tissue, especially in hyperplastic synovial tissue. PRDX4 silencing significantly inhibited the tumor cell-like behaviors and mRNA expression of matrix metalloproteinases (MMPs) in RA-FLS. Furthermore, overexpression of PRDX4 markedly activated PI3K/Akt signaling pathway, which can be reverted by Akt inhibitor MK-2206. These observations identified elevated PRDX4 may regulates the tumor cell-like biological characteristic of RA-FLS via Pi3k/Akt pathway. Targeting PRDX4 and its downstream signaling pathway might provide a potential diagnostic markers and therapeutic target for RA.
Keywords: Fibroblast-like synoviocytes; PRDX4; Pi3k/Akt signaling pathway; Rheumatoid arthritis.
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