Neutralisation of TGFβ or binding of VLA-4 to fibronectin prevents rat tendon adhesion following transection

Jørgensen, Heather G.; McLellan, Sarah; Crossan, J. F.; Curtis, Adam

doi:10.1016/j.cyto.2004.12.017

Cited by 39 publications

(30 citation statements)

References 25 publications

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“…Loading and mobilization of the tendon seem to decrease the expression of TGF-β (Eliasson et al, 2009), possibly reducing the initial inflammation in the healing tendon. At the end stage of tendon healing TGF-β may also promote the apoptosis of fibrocytes (Jorgensen et al, 2005;Lui et al, 2007). In our one studies we observe a high concentration of TGF-β initially, which then decreased for 2 and 4 weeks and then increase massively at 8 weeks, possibly reflecting the initial inflammation and activation of cells, followed by an intermediary period and then the remodeling of the tendon with increased apoptosis of no longer necessary cells.…”

Section: Tgf-βmentioning

confidence: 69%

Tendon Healing with Growth Factors

Müller¹,

Todorov²,

Heisterbach³

et al. 2012

Achilles Tendon

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Section: Tgf-βmentioning

confidence: 69%

Tendon Healing with Growth Factors

Müller¹,

Todorov²,

Heisterbach³

et al. 2012

Achilles Tendon

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“…3,[15][16][17][18] Other studies have focused on molecular treatment of the flexor tendon injury to provide adhesion-free healing via the delivery of anti-scarring adjuvants that inhibit the effects of TGF-b and bFGF among other factors. [19][20][21][22][23] Despite their promise, these approaches remain experimental and have yet to yield a clinical application, 3 largely because our understanding of the molecular mechanisms involved in the formation of adhesions after flexor tendon injury and grafting remains incomplete. The novel mouse model of FDL tendon grafts offers a quantitative tool to not only examine the biomechanical aspects of flexor tendon grafts, but also to potentially elucidate the molecular events involved in repair and subsequent adhesion formation via the use of transgenic mouse models of gain and loss of function.…”

Section: Discussionmentioning

confidence: 99%

Adhesions in a murine flexor tendon graft model: Autograft versus allograft reconstruction

Hasslund

Jacobson

Dadali

et al. 2008

Journal Orthopaedic Research

120

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Reconstruction of flexor tendons often results in adhesions that compromise joint flexion. Little is known about the factors involved in the formation of flexor tendon graft adhesions. In this study, we developed and characterized a novel mouse model of flexor digitorum longus (FDL) tendon reconstruction with live autografts or reconstituted freeze-dried allografts. Grafted tendons were evaluated at multiple time points up to 84 days post-reconstruction. To assess the flexion range of the metatarsophalangeal joint, we developed a quantitative outcome measure proportional to the resistance to tendon gliding due to adhesions, which we termed the Gliding Coefficient. At 14 days post-grafting, the Gliding Coefficient was 29-and 26-fold greater than normal FDL tendon for both autografts and allografts, respectively (p < 0.001), and subsequently doubled for 28-day autografts. Interestingly, there were no significant differences in maximum tensile force or stiffness between live autograft and freeze-dried allograft repairs over time. Histologically, autograft healing was characterized by extensive remodeling and exuberant scarring around both the ends and the body of the graft, whereas allograft scarring was abundant only near the graft-host junctions. Gene expression of GDF-5 and VEGF were significantly increased in 28-day autografts compared to allografts and to normal tendons. These results suggest that the biomechanical advantages for tendon reconstruction using live autografts over devitalized allografts are minimal. This mouse model can be useful in elucidating the molecular mechanisms in tendon repair and can aid in preliminary screening of molecular treatments of flexor tendon adhesions. ß

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“…Several growth factors including BMP, TGF-b, bFGF and PDGF have been shown to enhance wound healing process, increase cell proliferation and collagen production in rat tendon [23e25]. However, during the wound healing process, available growth factor concentration has to be precisely balanced so that it is neither insufficient to cause failure to induce repair nor excess to cause adhesion of the skin on tendon scar surface and the loss of normal tendon function [26]. In vivo gene transfer approach is also known to have major disadvantages such as the adversity of finding vectors with high transgenic activity, immune response development against vectors, and general safety concerns as in all gene therapy appli-…”

Section: Introductionmentioning

confidence: 99%