Platelet‑rich plasma promotes the migration and invasion of synovial fibroblasts in patients with rheumatoid arthritis.
Platelet‑rich plasma promotes the migration and invasion of synovial fibroblasts in patients with rheumatoid arthritis.
复制标题
富含血小板的血浆促进类风湿关节炎患者滑膜成纤维细胞的迁移和侵袭。
DOI：
10.3892/mmr.2016.5500
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发表时间：
2016
影响因子：
3.4
通讯作者：
Yu Zhang
中科院分区：
文献类型：
--
作者：
Shanshan Yan;Binzhou Yang;C. Shang;Zhongshuang Ma;Z. Tang;Guiping Liu;Weigan Shen;Yu Zhang
富血小板血浆(PRP)是一种富含血小板的血浆，其数量与类风湿活动度密切相关。PRP是自体血小板的集中来源，含有多种不同的生长因子和细胞因子，包括血小板衍生生长因子、转化生长因子-β和胰岛素样生长因子-1，它们可以促进骨和软组织的愈合。类风湿关节炎(RA)的特征是滑膜增生、细胞活化、关节炎症和滑膜侵入邻近的骨和软骨。成纤维样滑膜细胞(Fls)与细胞外基质(ECM)的黏附、迁移和侵袭是RA患者关节软骨侵蚀和破坏的重要原因。本研究旨在探讨PRP对RA-FLSS黏附、迁移和侵袭的影响。Scratch和Transwell迁移实验表明，浓度为2%和5%的PRP可显著增强RA-FLSS的迁移能力。用2%和5%的PRP处理RA-FLSS可促进细胞的黏附和侵袭。此外，免疫荧光分析显示，PRP导致RA-FLSS中中央定位的应力纤维数量减少，并导致可检测到的前沿突起中丝状足和片状脂膜的形成增加。此外，逆转录-定量聚合酶链式反应和Western印迹分析表明，PRP上调了基质金属蛋白酶-1(MMP1)的蛋白和mRNA表达水平。结论：PRP促进RA-FLS细胞在ECM上的迁移、侵袭和黏附可能是通过上调MMP1的表达和诱导肌动蛋白细胞骨架重组来实现的。
Platelet-rich plasma (PRP) is blood plasma that has been enriched with platelets, and the number of platelets is correlated with rheumatoid activity. PRP is a concentrated source of autologous platelets, and contains several different growth factors and cytokines, including platelet‑derived growth factor, transforming growth factor‑β and insulin‑like growth factor‑1, which stimulate healing of bone and soft tissue. Rheumatoid arthritis (RA) is characterized by synovial hyperplasia, cell activation, articular inflammation and invasion of the synovium into the adjacent bone and cartilage. The adhesion of fibroblast‑like synoviocytes (FLSs) onto the extracellular matrix (ECM), migration and invasion are important for the erosion and destruction of the articular cartilage of patients with RA. The aim of the present study was to investigate the effects of PRP on the adhesion, migration and invasion of RA‑FLSs. Scratch and Transwell migration assays determined that PRP at a concentration of 2 and 5% significantly enhanced the migration ability of RA‑FLSs. Treatment of RA‑FLSs with 2 and 5% PRP promoted the adhesion and invasion of the cells. Additionally, the immunofluorescence assay revealed that PRP induced a decrease in the number of centrally located stress fibers and led to an increase in the formation of filopodia and lamellipodia in the detectable leading edge protrusions in RA‑FLSs. In addition, reverse transcription‑quantitative polymerase chain reaction and western blot analysis determined that PRP upregulated the protein and mRNA expression levels of matrix metalloproteinase‑1 (MMP‑1). In conclusion, the promotion of RA‑FLS cell migration, invasion and adhesion on the ECM by PRP may be modulated through the upregulation of MMP‑1 expression and the induction of actin cytoskeletal reorganization.