Cross-talk between TGF-β/Smad pathway and Wnt/β-catenin pathway in pathological scar formation

• Published in: International journal of clinical and experimental pathology Vol. 8; no. 6; pp. 7631 - 7639
• Main Authors: Sun, Qiang, Guo, Shu, Wang, Chen-Chao, Sun, Xu, Wang, Di, Xu, Nan, Jin, Shi-Feng, Li, Ke-Zhu
• Format: Journal Article
• Language: English
• Published: United States e-Century Publishing Corporation 01.01.2015
• Subjects: Adult; Aged; beta Catenin - genetics; beta Catenin - metabolism; Blotting, Western; Case-Control Studies; Cells, Cultured; Cicatrix, Hypertrophic - genetics; Cicatrix, Hypertrophic - metabolism; Cicatrix, Hypertrophic - pathology; Female; Humans; Immunohistochemistry; Keloid - genetics; Keloid - metabolism; Keloid - pathology; Male; Middle Aged; Original; Real-Time Polymerase Chain Reaction; Skin - metabolism; Skin - pathology; Smad2 Protein - metabolism; Smad3 Protein - metabolism; Transforming Growth Factor beta1 - genetics; Transforming Growth Factor beta1 - metabolism; Wnt Signaling Pathway; Wnt1 Protein - metabolism; Young Adult; pathological scar; Wnt/β-catenin pathway; TGF-β/Smad pathway
• ISSN: 1936-2625

TGF-β1 is a key factor in the process of wound healing, which is regulated by TGF-β/Smad pathway. We previously demonstrated that TGF-β1 contributed to pathological scar formation. And previous studies also suggested Wnt/β-catenin pathway might be involved in wound healing. However, their role and relation in pathological scar formation remains not very clear. For evaluating TGF-β1 and β-catenin, key factors of the two signal pathways, immunohistochemistry, western blot analysis and RT-PCR were used. Simultaneously, immunohistochemistry were used to evaluate Smad2, Smad3 and Wnt-1, which were also the important factors. We found that they all significantly accumulated in pathological scars compared with normal skins (P<0.05), that implied the two signal pathways both contributed to pathological scar formation. Meanwhile, β-catenin expression showed a tendency to increase first and then decrease under the influence of different concentrations of TGF-β1 (P<0.01). It is possible that there is a complicated interaction between the two signal pathways in pathological scar formation (both synergy and antagonism).