Cross-talk between TGF-β/Smad pathway and Wnt/β-catenin pathway in pathological scar formation.
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).
Department of Plastic Surgery, The First Hospital of China Medical University Shenyang, China.
Qiang
Q
Sun
Department of Plastic Surgery, The First Hospital of China Medical University Shenyang, China.
Shu
S
Guo
Department of Plastic Surgery, The First Hospital of China Medical University Shenyang, China.
Chen-Chao
CC
Wang
Department of Plastic Surgery, The First Hospital of China Medical University Shenyang, China.
Xu
X
Sun
Department of Plastic Surgery, The First Hospital of China Medical University Shenyang, China.
Di
D
Wang
Department of Plastic Surgery, The First Hospital of China Medical University Shenyang, China.
Nan
N
Xu
Department of Plastic Surgery, The First Hospital of China Medical University Shenyang, China.
Shi-Feng
SF
Jin
Department of Plastic Surgery, The First Hospital of China Medical University Shenyang, China.
Ke-Zhu
KZ
Li
D000328:Adult; D000368:Aged; D015153:Blotting, Western; D016022:Case-Control Studies; D002478:Cells, Cultured; D017439:Cicatrix, Hypertrophic / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D007627:Keloid / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D060888:Real-Time Polymerase Chain Reaction; D012867:Skin / Q000378:metabolism* / Q000473:pathology; D051899:Smad2 Protein / Q000378:metabolism*; D051900:Smad3 Protein / Q000378:metabolism*; D053773:Transforming Growth Factor beta1 / Q000235:genetics / Q000378:metabolism*; D060449:Wnt Signaling Pathway; D051155:Wnt1 Protein / Q000378:metabolism*; D055815:Young Adult; D051176:beta Catenin / Q000235:genetics / Q000378:metabolism*
C495270:CTNNB1 protein, human; C497782:SMAD2 protein, human; C497790:SMAD3 protein, human; D051899:Smad2 Protein; D051900:Smad3 Protein; C508960:TGFB1 protein, human; D053773:Transforming Growth Factor beta1; C495247:WNT1 protein, human; D051155:Wnt1 Protein; D051176:beta Catenin
TGF-β/Smad pathway; Wnt/β-catenin pathway; pathological scar