论文摘要
背景:转化生长因子β（transforming growth factorβ,TGF-β）通过抑制角质形成细胞增殖在维持表皮内环境的稳定方面发挥重要作用。多种Smad蛋白参与了TGF-β信号从膜受体到细胞核的细胞内转导和调节。根据其序列特点和在信号转导中的功能,Smad可分为三类:受体活化Smad （the receptor-activated Smads,R-Smads）、共有Smad （the common-partner Smad,Co-Smad）和抑制性Smad （the inhibitory Smads,I-Smads）。寻常型银屑病是皮肤科临床上常见的慢性、复发性、炎症性皮肤病。多种细胞因子参与了其发病机制。其中,TGF-β信号转导障碍可能有助于银屑病皮损的形成。近年来的研究已发现,银屑病皮损表皮中存在着TGF-β/Smad信号转导途径的某些重要环节的异常,包括TGF-β及其受体的表达下调,而Smad泛素化调节因子（Smad ubiquitination regulatory factors,Smurf）和抑制性Smad之一——Smad7表达上调。基于上述研究发现,我们设想寻常型银屑病皮损表皮中还可能存在着Smad家族中其它重要成分之表达水平的改变。银屑病皮损中TGF-β受体活化Smad（Smad2和Smad3）和共有Smad（Smad4）表达水平有何变化尚不完全清楚。目的:探讨寻常型银屑病皮损中TGF-β受体活化Smad和共有Smad的表达特点及其意义,以进一步加深对TGF-β信号转导途径异常改变参与寻常型银屑病表皮过度增殖形成机制的理解。方法:应用反转录（RT）及实时定量聚合酶链式反应（Real time PCR）技术分别检测寻常型银屑病皮损区与正常对照皮肤中Smad2、Smad3和Smad4的mRNA表达水平。EliVisionTMplus免疫组织化学技术用于检测寻常型银屑病皮损与正常对照皮肤中Smad1/2/3、p-Smad2/3和Smad4蛋白的表达情况。结果:RT-Real time PCR分析显示,寻常型银屑病皮损区Smad2、Smad3和Smad4 mRNA表达水平较对照正常皮肤显著下调。免疫组化研究发现,与对照正常皮肤的表皮相比,寻常型银屑病皮损表皮中Smad1/2/3、p-Smad2/3和Smad4蛋白的表达水平也显著降低。结论:寻常型银屑病皮损表皮中存在着TGF-β受体活化Smad和共有Smad的表达下调。这些Smad表达下调可导致TGF-β信号下传受阻。在其它促炎症因素和促增殖因素的直接和间接作用下,失去TGF-β抑制作用的表皮角质形成细胞活跃地增殖且加速成熟,终致寻常型银屑病表皮增殖性病理改变的形成。本研究和既往研究结果提示银屑病皮损表皮中存在着TGF-β/Smad信号转导途径多个环节的异常。
论文目录
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