炎症
下调和上调
基因敲除
NF-κB
MAPK/ERK通路
成纤维细胞
信号转导
癌症研究
促炎细胞因子
类风湿性关节炎
p38丝裂原活化蛋白激酶
细胞凋亡
化学
免疫学
细胞生物学
医学
生物
生物化学
基因
体外
作者
Xin Zhang,He Nan,Jialong Guo,Jinyu Liu
出处
期刊:European Cytokine Network
[John Libbey Eurotext]
日期:2021-06-01
卷期号:32 (2): 15-22
被引量:7
标识
DOI:10.1684/ecn.2021.0465
摘要
Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease characterized by abnormal synovial hyperplasia and the release of inflammatory cytokines. NLRP12 is a member of the family nod-like receptor (NLR) families that are activators of inflammation. However, the role of NLRP12 in fibroblast-like synoviocytes (FLSs) is still unclear. In the present study, we have investigated the role of NLRP12 in fibroblast-like synoviocytes (FLSs). The results demonstrated that NLRP12 overexpression inhibited proliferation and promoted cell apoptosis in RA-FLSs. Moreover, NLRP12 overexpression repressed inflammation by downregulation of IL-1β, TNF-α, IL-6, IFN-γ and MCP-1 production and upregulation of IL-10 levels with knockdown of NLRP12 expression showing opposite effects. In addition, NLRP12 overexpression suppressed phosphorylation of JNK, ERK, p38 and NF-κB in RA-FLSs, whereas NLRP12 knockdown promoted phosphorylation of these proteins. In conclusion, these findings demonstrate that NLRP12 inhibits proliferation and inflammation of RA-FLSs via the regulation of the NF-κB and MAPK signaling pathways, suggesting that NLRP12 might be a potential target for RA treatment.
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