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. 2019 Aug;234(10):18748-18762.
doi: 10.1002/jcp.28514. Epub 2019 May 7.

CCR5 silencing reduces inflammatory response, inhibits viability, and promotes apoptosis of synovial cells in rat models of rheumatoid arthritis through the MAPK signaling pathway

You-Yu Lan  1   2 , You-Qiang Wang  3 , Yi Liu  1
Affiliations

CCR5 silencing reduces inflammatory response, inhibits viability, and promotes apoptosis of synovial cells in rat models of rheumatoid arthritis through the MAPK signaling pathway

You-Yu Lan et al. J Cell Physiol. 2019 Aug.

Retraction in

  • Retraction.
    [No authors listed] [No authors listed] J Cell Physiol. 2022 May;237(5):2599. doi: 10.1002/jcp.30740. Epub 2022 Apr 13. J Cell Physiol. 2022. PMID: 35416288

Abstract

Rheumatoid arthritis (RA) is a chronic inflammatory disorder that can, in severe cases, lead to disability. CC chemokine receptor (CCR), an integral membrane protein, has been suggested to play a key role in the RA developmentThis study is to explore the role of CCR5 silencing in inflammatory response, viability, and apoptosis of synovial cells in RA rats by inactivating the mitogen-activated protein kinase (MAPK) signaling pathway. Microarray analysis was conducted to screen out differentially expressed genes from RA-related chips. The rat model was established by injection of siRNA-CCR5 and PD98059 (inhibitor of mitogen-activated protein kinase kinase 1) to evaluate the role of CCR5 silencing in RA, with the involvement of inflammatory response, synovial cell viability, apoptosis, and cycle. CCR5 was predicted to participate in RA by regulating the MARK pathway. In animal experiments, reduction was identified in arthritis index (AI), CCR5 positive expression rate, levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), matrix metalloproteinase (MMP)-1, and MMP-3 in serum of RA rats after CCR5 siRNA and PD98059 injections. RA rats treated with CCR5 siRNA, and PD98059 presented with inhibition in cell viability, promotion of apoptosis, increase in cell proportion in G0/G1 phase, and shortened the S phase. In addition, the treatment of CCR5 siRNA, and PD98059 resulted in downregulated JNK1, ERK1, p38, Cyclin D1, Cyclin E1, Cyclin B1, and Bcl-2 and upregulated Bax and Cas3. These findings reveal that CCR5 silencing suppresses inflammatory response, inhibits viability, and promotes apoptosis of synovial cells in RA rats by inhibiting MAPK pathway. Therefore, CCR5 silencing may provide a novel therapeutic target for RA.

Keywords: CC chemokine receptor 5; MAPK signaling pathway; apoptosis; gene silencing; rheumatoid arthritis; synovial cells; viability.

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