Cyr61 Promotes Inflammation of a Gouty Arthritis Model in Rats

Autor: Mi Zhou, Kan Ze, Liang Hua, Liu Liu, Le Kuai, Ming Zhang, Bin Li, Yifei Wang, Xin Li
Jazyk: angličtina
Rok vydání: 2020
Předmět:
Zdroj: Mediators of Inflammation, Vol 2020 (2020)
Druh dokumentu: article
ISSN: 0962-9351
1466-1861
DOI: 10.1155/2020/8298615
Popis: Background. Cyr61 is considered a novel proinflammatory factor. Gouty arthritis (GA) is a self-limited inflammatory reaction caused by monosodium urate (MSU) crystals. In this study, we assessed the role of Cyr61 in the inflammatory process of GA. Methods. We investigated the expression of Cyr61 in MSU-induced rat gout models and MSU-stimulated rat fibroblast-like synovial (FLS) cells. After inhibiting the expression of Cyr61, levels of IL-1β, TNF-α, and IL-6 were detected by ELISA, qPCR, western blot, and immunohistochemical methods. We probed the downstream NF-κB signaling pathway using the NF-κB inhibitor PDTC, and levels of NF-κB and p-NF-κB were detected by western blot and qPCR. Results. Our results demonstrate that Cyr61 plays a potent role in the formation of local inflammation in vitro and in vivo. Cyr61 was highly expressed in synovial tissues of gout models, and the expression of Cyr61 protein was also significantly increased in MSU-stimulated FLS cells. Cyr61 promoted MSU-induced acute inflammation via the NF-κB signaling pathway. Conclusions. Our study has revealed that Cyr61 is an important regulatory factor for the initiation of inflammation in GA. The high expression of Cyr61 protein can induce synovial cells to produce many inflammatory cytokines, such as IL-1β, TNF-α, and IL-6, partly in an NF-κB-dependent manner. Thus, inhibition of Cyr61 could be a new target and strategy for the prevention and treatment of GA.
Databáze: Directory of Open Access Journals
Nepřihlášeným uživatelům se plný text nezobrazuje