[1]杨扬,何威,李颖,等.脂溢性角化病皮损区受体活化Smad的变化[J].陆军军医大学学报(原第三军医大学学报),2007,29(23):2219-2222.
 YANG Yang,HE Wei,LI Ying,et al.Down-regulation of receptor-activited Smads in seborrheic keratosis[J].J Amry Med Univ (J Third Mil Med Univ),2007,29(23):2219-2222.
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陆军军医大学学报(原第三军医大学学报)[ISSN:1000-5404/CN:51-1095/R]

卷:
29卷
期数:
2007年第23期
页码:
2219-2222
栏目:
论著
出版日期:
2007-12-15

文章信息/Info

Title:
Down-regulation of receptor-activited Smads in seborrheic keratosis
作者:
杨扬何威李颖何云志黄海林自华吴军杨进清
第三军医大学新桥医院皮肤科
Author(s):
YANG Yang HE Wei LI Ying HE Yun-zhi HUANG Hai LIN Zi-hua WU Jun YANG Jin-qing
Department of Dermatology, Xinqiao Hospital, Third Military Medical University
关键词:
脂溢性角化病转化生长因子β受体活化SmadSmad2Smad3p-Smad2/3信号通路
Keywords:
seborrheic keratosis TGF-β receptor-activited Smad Smad2 Smad3 p-Smad2/3 signal transduction pathway
分类号:
R329-33; R730.23; R739.5
文献标志码:
A
摘要:
目的  探讨转化生长因子β(transforming growth factor-β, TGF-β)信号转导通路中受体活化Smads(Smad2, Smad3)在脂溢性角化病皮损区的表达及其意义。  方法  采用反转录-实时定量聚合酶链式反应(RT and quantitative Real-Time PCR)和免疫组化技术分别检测脂溢性角化病皮损和正常对照皮肤中Smad2及Smad3的mRNA和Smad1/2/3及磷酸化Smad2/3(p-Smad2/3)蛋白的表达情况。  结果  与正常对照皮肤组相比,脂溢性角化病皮损中Smad2、Smad3 的mRNA以及Smad1/2/3、p-Smad2/3的表达水平下降。  结论  脂溢性角化病中受体活化Smads(Smad2、Smad3)和p-Smad2/3表达下调可阻断TGF-β信号转导,可能使TGF-β抑制上皮增生的作用不能有效发挥,从而促进了脂溢性角化病表皮的过度增生。
Abstract:
Objective  To investigate the expression of receptor-activited Smads (Smad2, Smad3) and phosphorylated Smad2,3 (p-Smad 2/3) in seborrheic keratosis.   Methods  The skin tissues of seborrheic keratosis from 45 patients (25 males and 20 females, average age: 57.6 years, average course of disease: 3.8 years) who received no treatment before and normal skin tissues from 40 patients (22 males and 18 females, average age: 48 years) undergoing plastic surgery in our hospital were examined for the mRNA levels of Smad2 and Smad3 by quantitative real-time PCR, and the protein levels of Smad1/2/3 and p-Smad2/3 by immunohistochemistry.   Results   The mRNA levels of receptor-activited Smads (Smad2, Smad3) and the protein levels of Smad1/2/3, p-Smad2/3 were significantly down-regulated in the skin tissues of seborrheic keratosis in comparison with control tissues.   Conclusion  Down-regulation of receptor-activited Smads (Smad2, Smad3) and p-Smad2/3 might interfere TGF-β signal transduction pathway and contribute to formation of aberrant hyperplastic epidermis in seborrheic keratosis.

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更新日期/Last Update: 2008-05-20