P57^(kip2)、PCNA、Ki67在银屑病皮损中的表达  

Expression of P57～(kip2),PCNA and Ki67 in psoriatic lesion

作　　者：张军民[1] 黄庚史[1] 周春红[1] 李伯有[1] 曾凡钦[1] 

机构地区：[1]中山大学附属第二医院皮肤科,广东广州510120

出　　处：《中国热带医学》2009年第3期453-454,共2页China Tropical Medicine

摘　　要：目的探讨有丝分裂抑制因子P57kip2、增殖细胞核抗原PCNA和Ki67蛋白表达在银屑病发病机制中的作用。方法以免疫组化S-P法检测44例寻常型银屑病皮损和10例正常表皮内P57kip2、PCNA、Kip67蛋白的表达水平。结果银屑病皮损内P57kip2,PCNA、Kip67蛋白表达率显著高于正常对照(P<0.05),阳性细胞分布在角朊细胞各层,正常表皮呈阴性或仅于基底层有弱阳性表达。结论银屑病皮损内存在细胞周期调控失常,这种不正常性与银屑病角朊细胞过度增殖和不正常分化相关,在银屑病的发病机制中起一定作用。Objective To investigate the role of P57^kip2 , proliferating cell nuclear antigen （PCNA） and Ki67 prtein in the pathogenesis of psoriasis. Methods The expression of P57^kip2 ,PCNA and Ki67 was determined by S-P immunohistochemical technique in the lesions of 44 patients with psoriasis vulgaris and in the epidermis of 10 normal controls. Results A higher positive-expression rate of Ki67,PCNA and P57^kip2 located in all layers of leisions of patients with psoriasis vulgaris was observed. There were no or only weak positive expressions in the basal layer of normal controls. Conclusions The overexpression of Ki67, PCNA and P57^kip2 in psoriatic leisions suggests that there is an ahnomality of cell cycle regulation of psoriatic kertinocytes.The abnomality might be related to the hyperproliferation and abnomal differentiation of psoriatic kertinoeytes, implying that it may be involved in the pathogenesis of psoriasis.

关 键 词：银屑病 P57^KIP2 PCNA KI67 

分 类 号：R758.63[医药卫生—皮肤病学与性病学]