Smad基因异常表达在银屑病发病机制中的临床意义  

Clinical significance of abnormal expression of Smad gene in pathogenesis of psoriasis

作　　者：翟慧娟[1] 杨廷桐[2] 李秀杰[3] 

机构地区：[1]新乡医学院第三附属医院皮肤性病科,新乡市453003 [2]新乡医学院病理教研室,新乡市453003 [3]新乡医学院诊断学实验室,新乡市453003

出　　处：《空军总医院学报》2010年第1期42-44,47,F0003,共5页Journal of General Hospital of Air Force,PLA

摘　　要：目的探讨银屑病皮损中Smad3、Smad4和Smad7的表达特点及其意义,进一步探讨TGF-β信号转导途径异常引起银屑病表皮过度增殖形成的机制。方法应用反转录(RT)聚合酶链式反应(Real ti me PCR)和免疫组织化学(I HC)技术分别检测银屑病皮损区与正常皮肤中Smad3、Smad4和Smad7的mRNA与蛋白表达水平。结果 RT-PCR和I HC分析显示,银屑病皮损区Smad3和Smad4表达水平较对照正常皮肤显著下降,而Smad7的表达水平较对照正常皮肤显著升高。(P<0.01)结论银屑病皮损表皮中TGF-β受体、活化Smad3和共有Smad4的表达下调,抑制性基因Smad7表达上调导致了TGF-β信号转导障碍,从而导致表皮角质形成细胞失去抑制作用,增殖活跃,加速其病理改变的形成。Objective To study the traits and significance of Smad3,Smad4 and Smad7 in skin lesions of psoriasis and to further understand the role of abnormal TGF-βsignal transduction in epidermis over-proliferation mechanism.Methods The expression level of mRNA and protein in Smad3,Smad4 and Smad7 in skin lesion part and normal skin were tested respectively by RT,Real time PCR and IHC.Results The expression level of Smad3 and Smad4 decreased greatly in skin lesions as compared with that in normal skin by RT-PCR and IHC analysis,while the expression level of Smad7 increased obviously.（p 0.01） Conclusion The result is caused by TCF-βand this leads to the difficulties in TGF-βsignal transduction as well.The hornylayerofepidermis without inhibiting effects results in the active proliferation of cells and rapid pathological changes.

关 键 词：银屑病/代谢 DNA结合蛋白质类 

分 类 号：R785.63[医药卫生—口腔医学]