银屑病皮损区c-myc、c-jun、Ki-67、PCNA、VEGF的表达

Expression of c-myc,c-jun,Ki-67,PCNA and VEGF in Psoriatic Lesions

目的 探讨原癌基因 c- m yc、c- jun、Ki- 6 7、细胞核增殖性抗原 (PCNA )、血管内皮细胞生长因子(VEGF)在银屑病发病中的作用。方法 采用免疫组化方法 ,检测了 32例寻常型银屑病皮损区及 5例正常人表皮中 c- myc、c- jun、Ki- 6 7、PCNA、VEGF的表达及分布特点。结果 银屑病皮损区 c- myc、c- jun、Ki- 6 7、PCNA、VEGF表达均较正常表皮中的表达明显增强 ,分布于除角质层以外的表皮各层 ,而正常表皮表达阴性或仅在基底层有弱阳性表达。结论 c- myc、c- jun、Ki- 6 7、PCNA在银屑病皮损中过度表达 ,提示其与银屑病的表皮细胞过度增殖、分化异常有关 ;VEGF过度表达 ,提示 VEGF与银屑病的真皮乳头毛细血管增生扩张、炎症细胞浸润有关。

Objective To investigate the effects of proto-oncogene c-myc, c-jun, Ki-67, proliferating cell nuclear antigen(PCNA) and vascular endothelial growth factor (VEGF) on the pathogenesis of psoriasis. Methods The expression and distribution of c-myc,c-jun,Ki-67,PCNA and VEGF were detected by immunohistochemistry in the lesions of 32 cases with psoriasis vulgaris and in the epidermis of 5 normal controls. Results The expressions of c-myc, c-jun, Ki-67, PCNA, VEGF in psoriatic epidermis were significantly higher than those in normal epidermis; they were located in all epidermal layers except horny layer. There were no or only weak positive expressions in the basal layer of normal controls. Conclusion The overexpressions of c-myc, c-jun, Ki-67 and PCNA in psoriatic epidermis suggest that they might be related to the hyperproliferation and abnormal differentiation of psoriatic keratinocytes, and the overexpression of VEGF suggests that VEGF might be related to dermal angiogenesis ,telangiectasis and inflammatory infiltration of psoriasis.