Jiang Ke, Chun Guo, Wang Ziming, Du Quanyin, Wang Aimin, Xiong Yan
Department of Orthopedics, Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan 637000, P.R. China.
Department of Medicine, Luohe Medical College, Luohe, Henan 462002, P.R. China.
Mol Med Rep. 2016 Apr;13(4):3567-73. doi: 10.3892/mmr.2016.4944. Epub 2016 Feb 29.
Tendon adhesion is a common problem in the healing of injured tendons. The molecular mechanisms of the TGF-β/Smad signaling pathway have been determined, and the role of TGF-β has been well characterized in wound healing. However, the intracellular mechanism or downstream signals by which TGF-β3 modulates its effects on tendon healing have not been well elucidated. The aim of this study was to determine the effect of TGF‑β3 on the TGF-β/Smad signaling pathway in tenocytes. Quantitative polymerase chain reaction and western blot analysis were used to analyze the effect of TGF‑β3 on the regulation of the expression of Smad proteins in tenocytes. The results demonstrated that TGF‑β3 has no significant effect on the proliferation of tendon cells. The addition of TGF‑β3 to tenocytes can significantly downregulate the expression of Smad3 and upregulate the expression of Smad7 at the gene and protein levels. The results demonstrate that TGF‑β3 may regulate Smad3 and Smad7 proteins through the TGF-β/Smad signaling pathway to minimize extrinsic scarring. Thus, it may provide a novel approach to decrease tendon adhesion and promote tendon healing.
肌腱粘连是肌腱损伤愈合过程中的常见问题。TGF-β/Smad信号通路的分子机制已被确定，并且TGF-β在伤口愈合中的作用也已得到充分表征。然而，TGF-β3调节其对肌腱愈合作用的细胞内机制或下游信号尚未得到很好的阐明。本研究的目的是确定TGF-β3对肌腱细胞中TGF-β/Smad信号通路的影响。采用定量聚合酶链反应和蛋白质印迹分析来分析TGF-β3对肌腱细胞中Smad蛋白表达调控的影响。结果表明，TGF-β3对肌腱细胞的增殖没有显著影响。向肌腱细胞中添加TGF-β3可在基因和蛋白质水平上显著下调Smad3的表达并上调Smad7的表达。结果表明，TGF-β3可能通过TGF-β/Smad信号通路调节Smad3和Smad7蛋白，以减少外在瘢痕形成。因此，它可能为减少肌腱粘连和促进肌腱愈合提供一种新方法。
