β-catenin和Dickkopf1在银屑病皮损中的表达

发布时间：2018-03-31 10:07

本文选题：银屑病　切入点：β-catenin　出处：《重庆医科大学》2012年硕士论文

【摘要】：背景：银屑病是一种病因不明的慢性、炎症性皮肤病，以其角质形成细胞的过度增生及异常分化为特点。有研究发现银屑病角质形成细胞的连接结构发生变化。 β-catenin是一种细胞间连接结构的成分，又是Wnt/β-catenin信号通路的转录因子。Wnt信号通过β-catenin调节表皮干细胞的增殖及分化。Dickkopf1（DKK1）作为负性调节因子可以阻断Wnt/β-catenin信号通路，抑制β-catenin的激活，，也调节间充质干细胞的分化。因此，我们推测β-catenin及其DKK1可能参与银屑病的增殖和分化过程。目的：检测β-catenin与DKK1在寻常型、脓疱型、红皮病型、关节病型4型银屑病及寻常型银屑病的进行期、静止期、退行期的皮损和正常表皮中的表达，探讨两者在银屑病中所起的作用。方法：用免疫组化方法检测63例银屑病皮损和20例正常表皮中β-catenin与DKK1的表达情况。结果：β-catenin在正常表皮全层的细胞膜上表达（100%），在银屑病中出现异常表达（58.73%），与正常表皮相比有差异（P0.01）。两组均未发现胞核或胞浆的易位。DKK1在正常表皮全层的胞浆中表达（100%），在银屑病中表达下降（69.84%），与对照组相比有表达差异（P0.05）。结论：β-catenin和DKK1可能参与银屑病的发病过程。DKK1的缺失可能导致Wnt/β-catenin信号通路的开启，通过激活β-catenin启动核基因，最终引起银屑病角质形成细胞的过度增生及分化不良。
[Abstract]:Background: psoriasis is a chronic inflammatory dermatosis with unknown etiology characterized by hyperproliferation and abnormal differentiation of keratinocytes. 尾 -catenin is a component of intercellular junctional structure. It is also a transcription factor of Wnt/ 尾 -catenin signaling pathway. Wnt signal regulates the proliferation and differentiation of epidermal stem cells by 尾 -catenin. As a negative regulatory factor, 尾 -catenin signal pathway is blocked and 尾 -catenin activation is inhibited. Therefore, we speculate that 尾 -catenin and its DKK1 may be involved in the proliferation and differentiation of psoriasis. Objective: to detect the expression of 尾 -catenin and DKK1 in psoriasis vulgaris, pustular psoriasis, erythroderma, arthropathy, psoriasis vulgaris and psoriasis vulgaris. To explore the role of both in psoriasis. Methods: the expression of 尾 -catenin and DKK1 in 63 cases of psoriatic lesions and 20 cases of normal epidermis were detected by immunohistochemical method. Results: 尾 -catenin was expressed on the membrane of the whole layer of normal epidermis. Abnormal expression of 尾 -catenin was found in psoriasis, which was different from normal epidermis (P 0.01). No translocation of nucleus or cytoplasm. DKK1 was found in the cytoplasm of the whole layer of normal epidermis. In psoriasis, the expression decreased 69.84%, compared with the control group, there was a difference in the expression of P0.05%. Conclusion: 尾 -catenin and DKK1 may be involved in the pathogenesis of psoriasis. The deletion of DKK1 may lead to the opening of Wnt/ 尾 -catenin signaling pathway, which may lead to the excessive proliferation and poor differentiation of keratinocytes in psoriatic patients by activating 尾 -catenin.
【学位授予单位】：重庆医科大学
【学位级别】：硕士
【学位授予年份】：2012
【分类号】：R758.63

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