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首页> 外文期刊>Rheumatology >Increased phosphorylation of ezrin is associated with the migration and invasion of fibroblast-like synoviocytes from patients with rheumatoid arthritis
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Increased phosphorylation of ezrin is associated with the migration and invasion of fibroblast-like synoviocytes from patients with rheumatoid arthritis

机译：ezrin磷酸化的增加与类风湿关节炎患者成纤维样滑膜细胞的迁移和侵袭有关

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Objective: Increasing evidence indicates that the cytoskeletal protein ezrin may play a critical role in cell motility. This study aims to investigate the role of ezrin in regulating the migration and invasion of fibroblast-like synoviocytes (FLSs) from patients with RA. Methods: Synovial tissues were obtained from 12 patients with RA and 6 with OA, and then FLSs were separated from synovial tissues. The expression of ezrin and phosphorylated ezrin (p-ezrin) was examined by Western blotting or IF staining. A specific inhibitor of ezrin phosphorylation and small interference RNAmediated ezrin knockdown were used to inhibit the phosphorylation of ezrin. Migration and invasion of FLSs in vitro were measured by the Boyden chamber assay. Results: Increased expression of p-ezrin protein was found in synovial tissue and FLSs in patients with RA compared with patients with OA. Stimulation with TNF-α and IL-1β increased ezrin phosphorylation in RA FLSs. Inhibition of p-ezrin protein by a specific inhibitor of phosphorylation of ezrin and small interfering RNA-mediated knockdown reduced in vitro migration and invasion, as well as actin stress fibre formation in RA FLS. Furthermore, rho kinase and p38 mitogen-activated protein kinase (MAPK) signal pathways were involved in the phosphorylation of ezrin and invasion of RA FLSs. Conclusion: Increased expression of p-ezrin may contribute to aberrant aggressive behaviours of RA FLSs, which are mediated by rho kinase and the p38 MAPK pathway. This suggests a novel strategy targeting phosphorylation of ezrin to prevent synovial invasiveness and joint destruction in RA.
机译：目的：越来越多的证据表明，细胞骨架蛋白ezrin可能在细胞运动中起关键作用。这项研究旨在探讨ezrin在调节类风湿性关节炎患者成纤维样滑膜细胞（FLSs）迁移和侵袭中的作用。方法：从12例RA患者和6例OA患者中获取滑膜组织，然后从滑膜组织中分离出FLS。通过蛋白质印迹或IF染色检查ezrin和磷酸化ezrin（p-ezrin）的表达。特异性的ezrin磷酸化抑制剂和小干扰RNA介导的ezrin敲低可用于抑制ezrin的磷酸化。通过Boyden室测定法测量了FLS的体外迁移和侵袭。结果：与OA患者相比，RA患者的滑膜组织和FLSs中p-ezrin蛋白表达增加。 TNF-α和IL-1β刺激可增加RA FLS中的ezrin磷酸化。通过特异性的ezrin磷酸化抑制剂和小干扰RNA介导的敲除作用抑制p-ezrin蛋白可减少RA FLS中的体外迁移和侵袭以及肌动蛋白应激纤维的形成。此外，rho激酶和p38丝裂原激活的蛋白激酶（MAPK）信号通路参与了ezrin的磷酸化和RA FLS的侵袭。结论：p-ezrin的表达增加可能是由rho激酶和p38 MAPK途径介导的RA FLS异常侵袭行为的原因。这表明靶向ezrin磷酸化的新策略可预防RA中的滑膜侵袭和关节破坏。

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