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富血小板血浆促进腱旁细胞体外迁移、增殖及 Scleraxis 和血管内皮生长因子的基因表达。

Platelet-Rich Plasma Promotes Migration, Proliferation, and the Gene Expression of Scleraxis and Vascular Endothelial Growth Factor in Paratenon-Derived Cells In Vitro.

机构信息

Department of Orthopaedic Surgery and Musculoskeletal Science, Graduate School of Medicine, Yokohama City University, Yokohama, Japan.

出版信息

Sports Health. 2019 Mar/Apr;11(2):142-148. doi: 10.1177/1941738118807479. Epub 2018 Oct 30.

DOI:10.1177/1941738118807479
PMID:30376405
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6391547/
Abstract

BACKGROUND

: Platelet-rich plasma (PRP) is a treatment option for tendon injury because of its effective tendon-healing properties. At the early stage of tendon repair, paratenon-derived cells (PDCs) are thought to play a more important role than tendon proper-derived cells (TDCs). However, there has been no study investigating the effects of PRP on PDCs.

HYPOTHESIS

: PRP promotes the migration, proliferation, and differentiation of PDCs in vitro.

STUDY DESIGN

: Controlled laboratory study.

METHODS

: TDCs and PDCs were isolated from the tendon proper and paratenon of rat Achilles tendons and were cultured to the third passage. PRP was prepared from the rats using the double-spin method. Third-passage TDCs and PDCs were cultured in Dulbecco's modified Eagle medium with 2% fetal bovine serum (control group) or 2% fetal bovine serum plus 5% PRP (PRP group), and cell migration, proliferation, and differentiation were evaluated. The relative mRNA expression levels of scleraxis (Scx), tenomodulin (Tnmd), collagen type I alpha 1 (Col1a1), collagen type III alpha 1 (Col3a1), and vascular endothelial growth factor A (VEGF) were examined by quantitative real-time reverse transcription polymerase chain reaction.

RESULTS

: The cell migration rate was significantly higher in the PDCs of the PRP group than in the control group (1.4-fold increase; P = 0.02). Cell proliferation was significantly higher in the PDCs of the PRP group (2.2-fold increase; P < 0.01). In the PDCs, the gene expression levels of Scx, Col1a1, and VEGF were significantly increased by PRP (Scx: 2.0-fold increase, P = 0.01; Col1a1: 5.3-fold increase, P = 0.01; VEGF: 7.8-fold increase, P = 0.01), but the gene expression level of Tnmd, a factor for tendon maturation, was significantly reduced by PRP (0.11-fold decrease; P = 0.02).

CONCLUSION

: In vitro PRP promoted migration, proliferation, and tenogenic differentiation with the upregulation of Scx in PDCs. PRP also upregulated the expression of the angiogenic marker VEGF.

CLINICAL RELEVANCE

: Our results suggest that PRP treatment in vitro may enhance the tendon-healing properties of PDCs at the initial stage of tendon repair.

摘要

背景

富血小板血浆(PRP)因其有效的肌腱愈合特性而成为治疗肌腱损伤的一种选择。在肌腱修复的早期阶段,被认为是腱旁组织来源的细胞(PDCs)比肌腱本身来源的细胞(TDCs)发挥更重要的作用。然而,目前还没有研究调查 PRP 对 PDCs 的影响。

假设

PRP 促进体外 PDCs 的迁移、增殖和分化。

研究设计

对照实验室研究。

方法

从大鼠跟腱的腱旁组织和肌腱中分离 TDCs 和 PDCs,并培养至第 3 代。使用双旋法从大鼠中制备 PRP。将第 3 代 TDCs 和 PDCs 分别培养在含 2%胎牛血清的 Dulbecco 改良 Eagle 培养基(对照组)或含 2%胎牛血清加 5% PRP 的培养基(PRP 组)中,评估细胞迁移、增殖和分化情况。通过实时定量逆转录聚合酶链反应检测 Scleraxis(Scx)、Tenomodulin(Tnmd)、胶原 I 型α 1(Col1a1)、胶原 III 型α 1(Col3a1)和血管内皮生长因子 A(VEGF)的相对 mRNA 表达水平。

结果

PRP 组 PDCs 的细胞迁移率明显高于对照组(增加 1.4 倍;P = 0.02)。PRP 组 PDCs 的细胞增殖明显更高(增加 2.2 倍;P < 0.01)。在 PDCs 中,PRP 显著增加了 Scx、Col1a1 和 VEGF 的基因表达水平(Scx:增加 2.0 倍,P = 0.01;Col1a1:增加 5.3 倍,P = 0.01;VEGF:增加 7.8 倍,P = 0.01),但成熟因子 Tnmd 的基因表达水平显著降低(降低 0.11 倍;P = 0.02)。

结论

体外 PRP 促进了 PDCs 的迁移、增殖和腱形成分化,并上调了 PDCs 中的 Scx。PRP 还上调了血管生成标志物 VEGF 的表达。

临床相关性

我们的结果表明,体外 PRP 治疗可能会在肌腱修复的初始阶段增强 PDCs 的肌腱愈合特性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b58/6391547/a60e42d3acb8/10.1177_1941738118807479-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b58/6391547/614acfc7da50/10.1177_1941738118807479-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b58/6391547/24ac9b236619/10.1177_1941738118807479-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b58/6391547/8de54132c8ae/10.1177_1941738118807479-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b58/6391547/53ef467bd9d2/10.1177_1941738118807479-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b58/6391547/a60e42d3acb8/10.1177_1941738118807479-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b58/6391547/614acfc7da50/10.1177_1941738118807479-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b58/6391547/24ac9b236619/10.1177_1941738118807479-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b58/6391547/8de54132c8ae/10.1177_1941738118807479-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b58/6391547/53ef467bd9d2/10.1177_1941738118807479-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b58/6391547/a60e42d3acb8/10.1177_1941738118807479-fig5.jpg

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