Down-regulated expression of Smad4 in lesional psoriatic epidermis

叶超然; 何威; 黎智; 杨进清; 吴军; 何云志; 黄海

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Down-regulated expression of Smad4 in lesional psoriatic epidermis

更新时间：2026-01-09

- Down-regulated expression of Smad4 in lesional psoriatic epidermis
- Journal of Army Medical University Vol. 30, Issue 4, Pages: 314-317(2008)
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  CLC： R322.991;R392.12;R758.63
- Published：2008
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叶超然,何威,黎智,杨进清,吴军,何云志,黄海.寻常性银屑病皮损区表皮Smad4表达下调[J].陆军军医大学学报(原第三军医大学学报),2008,30(04):314-317.

　YE Chao-ran,HE Wei,LI Zhi,YANG Jin-qing,WU Jun,HE Yun-zhi,HUANG Hai.Down-regulated expression of Smad4 in lesional psoriatic epidermis[J].J Amry Med Univ (J Third Mil Med Univ),2008,30(04):314-317.
叶超然,何威,黎智,杨进清,吴军,何云志,黄海.寻常性银屑病皮损区表皮Smad4表达下调[J].陆军军医大学学报(原第三军医大学学报),2008,30(04):314-317. DOI：

　YE Chao-ran,HE Wei,LI Zhi,YANG Jin-qing,WU Jun,HE Yun-zhi,HUANG Hai.Down-regulated expression of Smad4 in lesional psoriatic epidermis[J].J Amry Med Univ (J Third Mil Med Univ),2008,30(04):314-317. DOI：

摘要

目的探讨转化生长因子β(TGF-β)/Smad信号转导途径中共有Smad(Smad4)在寻常性银屑病皮损中的表达水平及其意义。方法采用反转录-实时定量聚合酶链式反应(Quantitative Real-Time RT-PCR)和免疫组化技术分别检测寻常性银屑病皮损和正常对照皮肤中Smad4 mRNA及其蛋白质的表达情况。结果寻常性银屑病皮损中Smad4 mRNA及其蛋白质表达水平显著低于正常对照皮肤。结论寻常性银屑病皮损表皮中Smad4表达下调可干扰TGF-β信号转导，有助于寻常性银屑病皮损中表皮增殖状态的形成。

Abstract

Objective To investigate the expression of common-partner Smad—Smad4 in psoriatic lesions. Methods The skin of psoriatic lesion from 21 patients visiting our out-patient clinic or admitted in Department of Dermatology of our hospital (13 males and 8 females

aged 10-67 years old

averaging 33.7) and the normal skin from 20 healthy subjects who underwent plastic surgery or bone surgery (13 males and 7 females

aged 13-59 years old

averaging 29.3). Quantitative real-time PCR and immunohistochemical technique were used to detect the expression levels of Smad4. Results The protein and mRNA expression levels of Smad4 were significantly lower in psoriatic lesions than those in normal control skin. Conclusion Down-regulated expressions of Smad4 in psoriatic epidermis might contribute to the formation of hyperplastic epidermis in psoriatic lesions through blocking TGF-β signal transduction.

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