Hall P A, McKee P H, Menage H D, Dover R, Lane D P
Department of Histopathology, UMDS, London, UK.
Oncogene. 1993 Jan;8(1):203-7.
Exposure of normal adult human skin to doses of UV irradiation that induced mild sunburn resulted in the rapid appearance of p53 protein in the epidermis and superficial dermal fibroblasts. Immunohistological analysis with a panel of antibodies established that while p53 staining was not seen in normal skin it appeared within 2 h of UV exposure. The level of p53 immunostaining peaked at 24 h and returned to undetectable levels within 360 h. The induction of proliferating cell nuclear antigen (PCNA) (which is required for both DNA replication and repair) followed a similar spatial and temporal pattern to p53. The UV irradiation did not induce a mitotic response or the replication-associated antigens DNA polymerase alpha or Ki67. The accumulation of high levels of p53 and PCNA in response to UV doses to which many human populations are routinely exposed provides strong support for a model in which normal p53 acts as part of the DNA damage response in vertebrate cells. Such a model is consistent with the profound tumour-suppressor function of the p53 gene, the high rate of p53 mutation in neoplasia and the exceptionally high tumour susceptibility of p53-deficient mice.
正常成年人皮肤暴露于能引起轻度晒伤的紫外线辐射剂量下,会导致表皮和真皮浅层成纤维细胞中p53蛋白迅速出现。用一组抗体进行免疫组织学分析表明,正常皮肤中未见p53染色,但在紫外线暴露后2小时内出现。p53免疫染色水平在24小时达到峰值,并在360小时内恢复到检测不到的水平。增殖细胞核抗原(PCNA)(DNA复制和修复都需要)的诱导与p53遵循相似的空间和时间模式。紫外线辐射未诱导有丝分裂反应或与复制相关的抗原DNA聚合酶α或Ki67。许多人群经常暴露于紫外线剂量下会导致高水平的p53和PCNA积累,这为正常p53作为脊椎动物细胞DNA损伤反应一部分的模型提供了有力支持。这样的模型与p53基因的深刻肿瘤抑制功能、肿瘤形成中p53的高突变率以及p53缺陷小鼠极高的肿瘤易感性相一致。