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P200 Beta-catenin causes fibrotic changes in the ECM via upregulation of collagen I transcription
( Mi Ryung Roh ),( Ji Young Choi ),( Raj Kumar ),( Apunchelvi Rajadurai ),( Jenny Njauw ),( Un Hee Ryoo ),( Kee Yang Chung ),( Hensin Tsao ) 대한피부과학회 2016 대한피부과학회 학술발표대회집 Vol.68 No.2
<div style="display:none">fiogf49gjkf0d</div><div style="display:none">fiogf49gjkf0d</div><div style="display:none">fiogf49gjkf0d</div><div style="display:none">fiogf49gjkf0d</div><div style="display:none">fiogf49gjkf0d</div><div style="display:none">fiogf49gjkf0d</div><div style="display:none">fiogf49gjkf0d</div> Background: Keloid scars represent a pathological response to cutaneous injury. They are characterized by increased proliferation of fibroblasts, especially in the active growth phase, as well as an abnormally increased production of collagen. The Wnt/β-catenin signaling pathway is a multifunctional network that plays an essential role in embryonic development, organogenesis, and tissue homeostasis. Objectives: We hypothesized that expression of stabilized β-catenin in fibroblasts is sufficient to cause fibrotic changes in the ECM via upregulation of collagen I transcription. Methods: First, we identified the expression of β-catenin and collagen in keloid tissues and cell lines. Then, we generated a tetracycline controlled stable immortalized fibroblast cell line expressing β-catenin to explore the role of stabilized β-catenin in collagen I transcription and synthesis. Results: By immunohistochemical staining, fibroblasts in keloid tissues showed significantly higher expression of β -catenin (p=0.046) and collagen I (p=0.002) than those of normal tissues. Immortalized fibroblasts with β-catenin overexpression (IF β-catenin) showed increased β -catenin, collagen I, and collagen III expression. Measurement of mRNA level by RT-PCR showed that β -catenin (p=0.02), col I (p=0.007), and col III (p=0.019) were markedly expressed in IF β-catenin compared to IF control. To determine if β-catenin had a direct transcriptional effect on the collagen I promoter, we generated a COL1A2-luciferase reporter and observed a dose-dependent increase in luciferase activity with increasing amounts of β-catenin. Conclusion: We found that the increased expression of β -catenin in fibroblasts is sufficient for increased collagen I synthesis, with concomitant increases in the COL1A2 luciferase activity. The highly increased levels of β -catenin together with its potent pro-fibrotic effects suggest that β-catenin might be a candidate for anti-fibrotic approaches.