Effect of TGF-beta Inducible Early Gene Deficiency on Flexor Tendon Healing
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Figure 1: Immunohistochemical analysis of TGF-beta.
Principal Investigator: Peter C. Amadio, M.D.
Project Coordinator: Chunfeng Zhao, M.D. — zhao.chunfeng@mayo.edu
Recent developments in genetic and molecular biology research provide opportunities to investigate the molecular events of tendon healing. TGF-beta regulates the events at various phases, such as inflammation, collagen production, angiogenesis, restoration of the gliding surface, and even adhesion formation. Regulating the role of TGF-beta therefore has the potential to improve the results of tendon repair by TGF-beta affects gene expression primarily by activation of the Smad signaling pathway. The first step in this pathway is expression of TGF-beta inducible early gene (TIEG). In this study, we compared the gene expression of TGF-beta1, beta2, beta3, collagen type I and type III in tissue cultured repaired flexor digitorum longus (FDL) tendons of TIEG 1 knockout mice with those of control mice. Both groups showed healing of the lacerated tendon, but the expression pattern of TGF-beta was different between the knockout and normal tendons. TIEG deficient tendons had delayed expression of TGF-beta, compared with control tendons. The collagen mRNA expression pattern was similar with both groups, but the expression level was different, with TIEG -/- tendons having less expression of collagen type I mRNA (Fig. 1).
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