Department of Bone Metabolism, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Laboratory for Dental Materials and Oral Tissue Regeneration, Shandong University, Wenhua West Road 44-1, Jinan, 250012, China.
Department of Endodontics, Jinan Stomatological Hospital, Jinan, 250001, China.
J Mol Histol. 2021 Aug;52(4):661-669. doi: 10.1007/s10735-021-09988-8. Epub 2021 Jun 3.
Rheumatoid arthritis (RA) is a chronic, progressive, and systemic inflammatory joint disease characterized by synovial inflammation and joint damage. Abnormal activation of fibroblast-like synoviocytes is an initial event of synovial inflammation and joint damage, which can significantly aggravate the progression of RA. Clinical studies have shown that synovitis may be associated with pyroptosis. Therefore, this study is mainly aim for exploring the underlying mechanisms of relationship between inflammation and pyroptosis during synovitis. A cell model of synovitis was constructed by stimulating synovial fibroblasts RSC-364 cells with lipopolysaccharide (LPS). In vitro, we found that LPS can induce pyroptosis of synovial fibroblasts through NOD-like receptor pyrin domain-3/caspase-1/gasdermin D and caspase-3/gasdermin E two signaling pathways, and these two signaling pathways can promote each other. In addition, NF-κB signaling pathway, as the upstream of these two pathways, is involved in regulating the pyroptosis of synovial fibroblast. These results suggest that pyroptosis may be triggered during the occurrence of RA. We hope to provide a new perspective for the study of RA and a new therapeutic target for clinical treatment of RA.
类风湿关节炎(RA)是一种慢性、进行性、系统性炎症性关节疾病,其特征为滑膜炎症和关节损伤。成纤维样滑膜细胞的异常激活是滑膜炎症和关节损伤的初始事件,可显著加重 RA 的进展。临床研究表明,滑膜炎可能与细胞焦亡有关。因此,本研究主要旨在探索滑膜炎中炎症与细胞焦亡之间关系的潜在机制。通过用脂多糖(LPS)刺激滑膜成纤维细胞 RSC-364 细胞来构建滑膜炎细胞模型。在体外,我们发现 LPS 可以通过 NOD 样受体 pyrin 结构域-3/半胱天冬酶-1/gasdermin D 和半胱天冬酶-3/ gasdermin E 两条信号通路诱导滑膜成纤维细胞发生细胞焦亡,并且这两条信号通路可以相互促进。此外,NF-κB 信号通路作为这两条通路的上游,参与调节滑膜成纤维细胞的细胞焦亡。这些结果提示细胞焦亡可能在 RA 的发生过程中被触发。我们希望为 RA 的研究提供新的视角,并为 RA 的临床治疗提供新的治疗靶点。