Can platelet-rich plasma enhance tendon repair? A cell culture study
Can platelet-rich plasma enhance tendon repair? A cell culture study
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DOI：
10.1177/0363546508314430
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发表时间：
2008-06-01
影响因子：
4.8
通讯作者：
van Osch, Gerjo J. V. M.
中科院分区：
文献类型：
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作者：
de Mos, Marieke;van der Windt, Anna E.;van Osch, Gerjo J. V. M.
背景：自体富血小板血浆（PRP）应用似乎可以改善外伤性肌腱损伤的肌腱愈合，但PRP如何促进肌腱修复的基础知识是必要的。假设：富血小板血浆对细胞增殖和胶原生成有积极作用，诱导人细胞产生基质降解酶和内源性生长因子。研究设计：实验室对照研究。方法：将人细胞在2%胎牛血清培养基中培养14天，培养基中分别添加0%、10%或20%体积/体积富血小板凝块释放物（PRP的活性释放物）或血小板贫凝块释放物（PPCR）。在第4、7、14天，分析细胞数量、总胶原、胶原α - 1 （COL1）、il - α - 1 （COL3）、基质金属蛋白酶（[MMPs] MMP1、MMP3、mmp13）、血管内皮源性生长因子(VEGF)-A、转化生长因子(TGF)- β 1的基因表达。结果：PRP患者血小板数量增加至基线的2.55倍。PRCR中VEGF和血小板衍生生长因子(PDGF)-BB的生长因子浓度高于PPCR。PRCR和PPCR均增加了细胞数量和总胶原蛋白，降低了COL-1和COO的基因表达，但不影响COL3/COL1比值。PRCR上调MMP1和MMP3的表达，而PPCR不上调。两种处理均未改变基质金属蛋白酶13的表达。PRCR增加了所有时间点的VEGF-A表达和第4天的tgf - β 1表达。结论：在人细胞培养中，PRCR和PPCR均能促进细胞增殖和总胶原蛋白的生成。而PPCR对基质降解酶和内源生长因子的表达有轻微的促进作用。临床意义：在肌腱损伤中，在体内使用PRP，以及在一定程度上使用PPP，可能会加速创伤损伤肌腱基质的分解代谢划分，促进血管生成和纤维血管愈伤组织的形成。这是否对退行性肌腱病也有益还有待阐明。
Background: Autologous platelet-rich plasma (PRP) application appears to improve tendon healing in traumatic tendon injuries, but basic knowledge of how PRP promotes tendon repair is needed.Hypothesis: Platelet-rich plasma has a positive effect on cell proliferation and collagen production and induces the production of matrix-degrading enzymes and endogenous growth factors by human tenocytes.Study Design: Controlled laboratory study.Methods: Human tenocytes were cultured 14 days in 2% fetal calf serum medium complemented with 0%, 10%, or 20% vol/vol platelet-rich clot releasate ([PRCR] the active releasate of PRP) or platelet-poor clot releasate (PPCR). At day 4, 7, and 14, cell amount, total collagen, and gene expression of collagen l alpha 1 (COL1) and IIl alpha 1 (COL3), matrix metalloproteinases ([MMPs] MMP1, MMP3, and MMP1 3), vascular endothelial-derived growth factor (VEGF)-A, and transforming growth factor (TGF)-beta 1 were analyzed.Results: Platelet numbers in PRP increased to 2.55 times baseline. Growth-factor concentrations of VEGF and platelet-derived growth factor (PDGF)-BB were higher in PRCR than PPCR. Both PRCR and PPCR increased cell number and total collagen, whereas they decreased gene expression of COL-1 and COO without affecting the COL3/COL1 ratio. PRCR, but not PPCR, showed upregulation of MMP1 and MMP3 expression. Matrix metalloproteinase 13 expression was not altered by either treatment. PRCR increased VEGF-A expression at all time points and TGF-beta 1 expression at day 4.Conclusion: In human tenocyte cultures, PRCR, but also PPCR, stimulates cell proliferation and total collagen production. PRCR, but not PPCR, slightly increases the expression of matrix-degrading enzymes and endogenous growth factors.Clinical Relevance: In vivo use of PRP, but also of PPP to a certain extent, in tendon injuries might accelerate the catabolic demarcation of traumatically injured tendon matrices and promote angiogenesis and formation of a fibrovascular callus. Whether this will also be beneficial for degenerative tendinopathies remains to be elucidated.