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自体富血小板凝块释放物刺激成年大鼠肌腱干细胞增殖并抑制其向非肌腱细胞谱系分化。

Autologous platelet-rich clot releasate stimulates proliferation and inhibits differentiation of adult rat tendon stem cells towards nontenocyte lineages.

作者信息

Chen L, Dong S-W, Tao X, Liu J-P, Tang K-L, Xu J-Z

机构信息

Department of Orthopaedics, Southwest Hospital, and Department of Anatomy, Third Military Medical University, Chongqing, China.

出版信息

J Int Med Res. 2012;40(4):1399-409. doi: 10.1177/147323001204000418.

DOI:10.1177/147323001204000418
PMID:22971491
Abstract

OBJECTIVE

To explore the effects of autologous platelet-rich clot releasate (PRCR) on proliferation and differentiation of adult rat tendon stem cells (TSCs) in vitro, following intense mechanical stretching.

METHODS

TSCs were subjected to 8% mechanical stretching and subsequently incubated in control medium or medium supplemented with 2% or 10% PRCR. Collagen types I and III, peroxisome proliferator-activated receptor-γ (PPARγ), sex determining region Y-box 9 (SOX-9) and runt-related transcription factor 2 (RUNX2) concentrations were assessed via Western blotting and flow cytometry. Transforming growth factor (TGF)-β1 and vascular endothelial growth factor concentrations were measured using enzyme-linked immunosorbent assay. Treated TSCs were also cultured in adipogenic, chondrogenic or osteogenic culture media.

RESULTS

PRCR increased the number of TSCs, and the concentrations of collagen types I and III and TGF-β1. In contrast, PRCR significantly reduced PPARγ, SOX-9 and RUNX2-positive cell numbers, and significantly reduced the numbers of TSC-derived adipocytes, chondrocytes and osteocytes.

CONCLUSION

PRCR induced tenocyte differentiation while suppressing the adipocyte, chondrocyte and osteocyte lineages believed to impede tendon healing.

摘要

目的

探讨自体富血小板凝块释放物(PRCR)对成年大鼠肌腱干细胞(TSCs)在体外受到强烈机械拉伸后增殖和分化的影响。

方法

对TSCs施加8%的机械拉伸,随后在对照培养基或添加2%或10%PRCR的培养基中培养。通过蛋白质印迹法和流式细胞术评估I型和III型胶原蛋白、过氧化物酶体增殖物激活受体-γ(PPARγ)、性别决定区Y盒9(SOX-9)和 runt相关转录因子2(RUNX2)的浓度。使用酶联免疫吸附测定法测量转化生长因子(TGF)-β1和血管内皮生长因子的浓度。处理后的TSCs也在成脂、成软骨或成骨培养基中培养。

结果

PRCR增加了TSCs的数量,以及I型和III型胶原蛋白和TGF-β1的浓度。相比之下,PRCR显著减少了PPARγ、SOX-9和RUNX2阳性细胞的数量,并显著减少了TSC衍生的脂肪细胞、软骨细胞和骨细胞的数量。

结论

PRCR诱导肌腱细胞分化,同时抑制被认为会阻碍肌腱愈合的脂肪细胞、软骨细胞和骨细胞谱系。

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