Neutralisation of TGF beta or binding of VLA-4 to fibronectin prevents rat tendon adhesion following transection.

ATMU & Division of Cancer Sciences, University of Glasgow, Level 3 Queen Elizabeth Building, UK.
Cytokine (Impact Factor: 2.87). 06/2005; 30(4):195-202. DOI: 10.1016/j.cyto.2004.12.017
Source: PubMed

ABSTRACT 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.

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    • "Transforming growth factor-Beta (TGF-β) is a potent fibrotic agent. Its inhibition with neutralizing antibodies has been shown to significantly reduce fibronectin concentrations and adhesion formation during early wound healing (Jorgensen et al., 2005). TGF-β1 has been shown to tilt gene expression in favour of ECM synthesis rather than matrix-remodelling matrix metalloproteinases , providing a mechanism for its promotion of adhesion formation (Farhat et al., 2012). "
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