Neutralisation of TGFβ or binding of VLA-4 to fibronectin prevents rat tendon adhesion following transection
Neutralisation of TGFβ or binding of VLA-4 to fibronectin prevents rat tendon adhesion following transection
复制标题
DOI：
10.1016/j.cyto.2004.12.017
复制
发表时间：
2005-05-21
期刊：
影响因子：
3.8
通讯作者：
Curtis, ASG
中科院分区：
文献类型：
--
作者：
Jorgensen, HG;McLellan, SD;Curtis, ASG
肌腱损伤后，由于滑膜管被纤维性瘢痕组织闭塞或修复后的肌腱断裂，经常会发生严重的功能丧失。细胞工程在肌腱修复中的作用是促进肌腱的牢固和快速愈合，同时促进滑膜管的快速重建。已发现改善愈合肌腱周围的即时炎症反应是有价值的。在实验上，这已经通过在损伤后的前3天中和转化生长因子β，或通过在肌腱横断的大鼠模型中用抗VLA-4抗体或用合成的VLA-4抑制剂CS-1肽阻断炎性细胞与纤连蛋白上的CS-1位点的结合来实现。从这项初步研究中得出的结论是，所描述的治疗方法有望改善人类肌腱损伤这一常见临床问题的结局。（c）2005 Elsevier Ltd.保留所有权利。
Following tendon injury, severe loss of function often occurs either as a result of obliteration of the synovial canal with fibrous scar tissue or from rupture of the repaired tendon. The role of cell engineering in tendon repair is to promote strong and rapid healing of tendon whilst at the same time facilitating rapid reconstitution of the synovial canal. Modification of the immediate inflammatory response around healing tendon has been found to be of value. Experimentally this has been achieved by neutralisation of transforming growth factor-beta over the first 3 days following injury, or by blockade of inflammatory cell binding to the CS-1 locus on fibronectin with an anti-VLA-4 antibody, or with the synthetic VLA-4 inhibitor, CS-1 peptide, in a rat model of tendon transection. It is concluded from this pilot study that the treatments described hold promise in improving outcomes of the common clinical problem of tendon injury in man. (c) 2005 Elsevier Ltd. All rights reserved.