Autologous Platelet-rich Clot Releasate Stimulates Proliferation and Inhibits Differentiation of Adult Rat Tendon Stem Cells Towards Nontenocyte Lineages

被引:27
作者
Chen, L. [1 ,2 ]
Dong, S-W [3 ]
Tao, X. [1 ]
Liu, J-P [1 ]
Tang, K-L [1 ]
Xu, J-Z [1 ]
机构
[1] Third Mil Med Univ, Dept Orthopaed, Southwest Hosp, Chongqing 400038, Peoples R China
[2] Wuhan Gen Hosp Guangzhou Mil Command, Dept Orthopaed, Wuhan, Hubei, Peoples R China
[3] Third Mil Med Univ, Dept Anat, Chongqing 400038, Peoples R China
基金
美国国家科学基金会;
关键词
DIFFERENTIATION; PLATELET-RICH CLOT RELEASATE; TENDINOPATHY; TENDON STEM CELLS; TRANSFORMING GROWTH FACTOR-beta 1; VASCULAR ENDOTHELIAL GROWTH FACTOR; ANTERIOR CRUCIATE LIGAMENT; ENDOTHELIAL GROWTH-FACTOR; PLASMA; EXPRESSION; REPAIR; TENDINOPATHY; PATHOGENESIS; FIBROBLASTS; CULTURE; MATRIX;
D O I
10.1177/147323001204000418
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
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-gamma (PPAR gamma), 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)-beta(1) 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-beta(1). In contrast, PRCR significantly reduced PPAR gamma, 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.
引用
收藏
页码:1399 / 1409
页数:11
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