RESUMO
BACKGROUND: In aged people, tendon injuries frequently occur during sporting and daily activities. In clinical practice, typical physiotherapeutic, pharmacotherapeutic, and surgical techniques do not result in the full recovery of injured tendons, which may lead to chronic degenerative disease. METHODS: We first isolated tendon stem cells (TSCs) from rats and transfected them with the TGFß1 gene, resulting in TGFß1-TSCs. The proliferation of TSCs was detected using the Cell Counting Kit 8, and TSCs were identified by immunofluorescence analysis and differentiation capacity analysis. Aggrecan, COL2A1, alpha smooth muscle actin (α-SMA), and p-Smad2 expression levels were detected using western blotting and quantitative reverse transcription polymerase chain reaction. Additionally, a tendon injury model was generated to explore the effect of TGFß1 on the repair of the tendon by TSCs. RESULTS: Compared with fibrinogen treatment, TSC + fibrinogen or TGFß1-TSC + fibrinogen treatment significantly promoted the fibrosis of injured tendons, as evidenced by histological analyses, with TGFß1-TSC + fibrinogen having a greater effect than TSC + fibrinogen. In TGFß1-TSCs, increased expression levels of aggrecan and COL2A1 indicated that TGFß1 signaling induced chondrogenic differentiation. Meanwhile, the increased collagen and α-SMA protein levels indicated that TGFß1 promoted fibrogenesis. Additionally, TGFß1 stimulated the production of phosphorylated Smad2 in TSCs, which suggested that the chondrogenic and fibrogenic differentiation of TSCs, as well as tissue regeneration, may be associated with the TGFß1/Smad2 pathway. CONCLUSION: TGFß1-TSC therapy may be a candidate for effective tendon fibrosis.
