Wnt5a is involved in the pathogenesis of cutaneous lichen planus. (10th January 2015)

• Record Type: Journal Article
• Authors: Zhang, Y.; Zhang, D.; Tu, C.; Zhou, P.; Zheng, Y.; Peng, Z.; Feng, Y.; Xiao, S.; Li, Z.
• Is Part Of: Clinical and experimental dermatology. Volume 40:Number 6(2015)
• Page Start: 659
• Page End: 664
• Publication Date: 2015-01-10
• Subjects: Skin -- Diseases -- Periodicals; 616.5
• DOI: 10.1111/ced.12561
• Languages: English
• ISSNs: 0307-6938

Abstract

<abstract abstract-type="main" id="ced12561-abs-0001"> <title>Summary</title> <sec id="ced12561-sec-0001" sec-type="section"> <title>Background</title> <p>Cutaneous lichen planus (CLP) is a chronic inflammatory and immune‐mediated disease. Wnt5a is one of the most extensively studied Wnt proteins, and has important functions in stimulating inflammation, cell proliferation, cell fate determination and cell differentiation. Wnt5a expression in CLP has not been comprehensively studied to date.</p> </sec> <sec id="ced12561-sec-0002" sec-type="section"> <title>Aim</title> <p>To determine the expression and distribution of Wnt5a in CLP.</p> </sec> <sec id="ced12561-sec-0003" sec-type="section"> <title>Methods</title> <p>Skin samples were obtained from patients with CLP and healthy controls (HCs). The <italic>WNT5A</italic> gene was detected by real‐time quantitative PCR, and Wnt5a protein by immunohistochemical analysis and western blotting.</p> </sec> <sec id="ced12561-sec-0004" sec-type="section"> <title>Results</title> <p> <italic>WNT5A </italic>mRNA was upregulated in CLP samples compared with the HC skin samples (<italic>P</italic> < 0.001). Wnt5a protein was overexpressed in all layers of the epidermis and dermis in CLP lesions compared with HC skin (all <italic>P</italic> < 0.001). These results were confirmed by western blotting.</p> </sec> <sec id="ced12561-sec-0005" sec-type="section"> <title>Conclusions</title> <p>The data presented in this study suggest that Wnt5a pathway may play an important role in the pathogenesis of CLP.</p> </sec> </abstract>