Association of Down-regulation of CD109 Expression with Up-expression of Smad7 in Pathogenesis of Psoriasis

• Published in: Journal of Huazhong University of Science and Technology. Medical sciences Vol. 36; no. 1; pp. 132 - 136
• Main Author: 刘欣欣 冯爱平 和义敏 李延 吴艳 连昕 胡枫 李家文 涂亚庭 陈善娟
• Format: Journal Article
• Language: English
• Published: Wuhan Huazhong University of Science and Technology 01.02.2016; Department of Dermatology,Union Hospital,Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430022,China
• Subjects: Adolescent; Adult; Antigens, CD - genetics; Antigens, CD - metabolism; Case-Control Studies; Down-Regulation; Female; GPI-Linked Proteins - genetics; GPI-Linked Proteins - metabolism; Humans; Male; Medicine; Medicine & Public Health; Middle Aged; Neoplasm Proteins - genetics; Neoplasm Proteins - metabolism; Psoriasis - metabolism; Psoriasis - pathology; Signal Transduction; Smad7 Protein - genetics; Smad7 Protein - metabolism; Transforming Growth Factor beta - metabolism; Up-Regulation; 临床; 医学; 症状; 诊断; transforming growth factor beta; signal transduction; psoriasis; CD109; Smad7
• ISSN: 1672-0733; 1993-1352; 1993-1352
• DOI: 10.1007/s11596-016-1555-1

Transforming growth factor（TGF）-β signaling plays an important role in the pathogenesis of psoriasis. CD109, a novel TGF-β co-receptor, which inhibits TGF-β signaling by enhancing Smad7-dependent degradation of TGF-β type Ⅰ receptor（TGF-β RⅠ）, is abnormally expressed in psoriasis. To date, the expression of Smad7 and the correlation between CD109 and Smad7 expression in psoriasis have not been fully elucidated. This study was designed to investigate the expression and the correlation of CD109 and TGF-β signaling associated proteins in psoriasis and their roles in the pathogenesis of psoriasis. Thirty-two psoriasis specimens were subjected to immunohistochemical staining for CD109, Smad7, TGF-β RⅠ and Ki67. Ten normal skin（NS） specimens served as controls. The positive expression rate（% positive cells） of Smad7 and Ki67 in psoriasis was significantly higher than in NS（62.6%±19.9% vs. 17.2%±4.4%, and 50.7%±14.3% vs. 19.5%±3.2%, respectively, P〈0.001）, and the expression levels of CD109 and TGF-β RⅠ were reduced significantly in psoriasis as compared with NS（8.1%±6.7% vs. 35.8%±6.7% and 27.3%±3.4% vs. 3.0%±3.4%, respectively, P〈0.001）. There were significantly negative correlations between CD109 and Smad7（r=-0.831, P〈0.01）. These findings indicated that CD109 might play a certain role in the pathogenesis of psoriasis. Lower expression of CD109 and TGF-β RⅠ was highly correlated with higher expression of Smad7 and Ki67, suggesting that CD109 may induce the pathogenesis of psoriasis through Smad7-mediated degradation of TGF-β RⅠ, and lead to the termination of TGF-β signaling.