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{"title":"Platelet rich plasma promotes skeletal muscle cell migration in association with up-regulation of FAK, paxillin, and F-Actin formation","authors":"Wen-Chung Tsai, Tung-Yang Yu, Li-Ping Lin, Mioa-Sui Lin, Ting-Ta Tsai, Jong-Hwei S. Pang","doi":"10.1002/jor.23547","DOIUrl":null,"url":null,"abstract":"<div>\n \n \n <section>\n \n <p>Platelet rich plasma (PRP) contains various cytokines and growth factors which may be beneficial to the healing process of injured muscle. The aim of this study was to investigate the effect and molecular mechanism of PRP on migration of skeletal muscle cells. Skeletal muscle cells intrinsic to Sprague–Dawley rats were treated with PRP. The cell migration was evaluated by transwell filter migration assay and electric cell-substrate impedance sensing. The spreading of cells was evaluated microscopically. The formation of filamentous actin (F-actin) cytoskeleton was assessed by immunofluorescence staining. The protein expressions of paxillin and focal adhesion kinase (FAK) were assessed by Western blot analysis. Transfection of paxillin small-interfering RNA (siRNAs) to muscle cells was performed to validate the role of paxillin in PRP-mediated promotion of cell migration. Dose-dependently PRP promotes migration of and spreading and muscle cells. Protein expressions of paxillin and FAK were up-regulated dose-dependently. F-actin formation was also enhanced by PRP treatment. Furthermore, the knockdown of paxillin expression impaired the effect of PRP to promote cell migration. It was concluded that PRP promoting migration of muscle cells is associated with up-regulation of proteins expression of paxillin and FAK as well as increasing F-actin formation. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 35:2506–2512, 2017.</p>\n </section>\n </div>","PeriodicalId":16650,"journal":{"name":"Journal of Orthopaedic Research®","volume":"35 11","pages":"2506-2512"},"PeriodicalIF":2.3000,"publicationDate":"2017-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/jor.23547","citationCount":"22","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Orthopaedic Research®","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/jor.23547","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"ORTHOPEDICS","Score":null,"Total":0}
引用次数: 22
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富血小板血浆与FAK、paxillin和F-Actin形成上调相关,促进骨骼肌细胞迁移
富血小板血浆(PRP)含有多种细胞因子和生长因子,可能有利于损伤肌肉的愈合过程。本研究旨在探讨PRP对骨骼肌细胞迁移的影响及其分子机制。PRP处理Sprague-Dawley大鼠骨骼肌细胞。通过transwell过滤器迁移实验和电-基底阻抗传感来评估细胞迁移。显微镜下观察细胞的扩散情况。免疫荧光染色观察丝状肌动蛋白(F-actin)细胞骨架的形成。Western blot检测paxillin和focal adhesion kinase (FAK)蛋白的表达。将paxillin小干扰RNA (sirna)转染到肌肉细胞中,以验证paxillin在prp介导的促进细胞迁移中的作用。剂量依赖性PRP促进肌肉细胞的迁移和扩散。paxillin和FAK蛋白表达呈剂量依赖性上调。PRP处理也促进了f -肌动蛋白的形成。此外,抑制paxillin的表达会削弱PRP促进细胞迁移的作用。由此可见,PRP促进肌肉细胞迁移与上调paxillin和FAK蛋白的表达以及增加F-actin的形成有关。©2017骨科研究学会。Wiley期刊公司出版。[J]中华骨科杂志,2017,35(5):2506 - 2512。
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