Abstract

Among hand injuries, exor tendon lacerations remain a challenge for hand surgeons. There are presently no therapeutic agents available for the prevention of tendon adhesions. It is already known that TGF-1 plays a role in tendon healing as well as in adhesion formation. Anti-TGF-1 therapies are not eective in preventing adhesion formation. The goal of the present study was to identify possible genes that are aected by TGF-1 in human Flexor Digitorum Profundus (FDP) tendon cells (tenocytes) in vitro. Tenocytes were isolated from human FDP tendons and treated with TGF-1 in low-serum cell culture medium. Gene expression was assessed at 6h and 24h using RTPCR. TGF-1 caused upregulation of several genes (SERPINE1, PLAU, ACTA2, CTGF, FN1, COL1A1, COL3A1, LOX, COMP, MMP13, TIMP1, TIMP3, BGN, SCX, POSTN, SMAD7, IL6, IGF1), downregulation of MMP9, DCN and ACAN, and had no eect on MMP2 and TIMP2. Targeting TGF-1-aected genes may be an alternative therapeutic approach in controlling adhesion formation that may lead to optimal healing of injured FDP tendon or FDP tendon graft.

Highlights

  • In cultured human Flexor Digitorum Profundus (FDP) tenocytes, we showed that Transforming Growth Factor-β1 (TGF-β1) induced Cartilage Oligomeric Matrix Protein (COMP) mRNA expression 3.4 and 17.1 fold at 6h and 24h respectively indicating its possible role in FDP tendon healing and fibrosis in vivo (Figure 2i)

  • The current study showed that TGF-β1 decreased MMP9 gene expression and increased TIMP1 gene expression in FDP tenocytes, in cell culture (Figure 3b,3d), indicating that fibrotic behavior in FDP tendon healing or repair may be modulated in vivo by TGF-β1 level

  • The present study investigated the effect of TGF-β1 (5 ng/ml) on the expression of several genes in FDP tenocytes in cell culture at 6h and 24h

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Summary

Objectives

The goal of the present study was to identify possible genes that are affected by TGF-β1 in human Flexor Digitorum Profundus (FDP) tendon cells in vitro

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