Yazici Ayça Cordan, Karabulut Ayşe Anil, Ozen Ozlem, Ekşioğlu Meral, Ustün Hüseyin
Department of Dermatology, Faculty of Medicine, Mersin University, Mersin, Turkey.
J Dermatol. 2007 Jun;34(6):367-74. doi: 10.1111/j.1346-8138.2007.00290.x.
Psoriasis is a common inflammatory and hyperproliferative skin disease characterized by hyperproliferation of keratinocytes. The pathogenesis of psoriasis has yet to be determined. The control of cell growth is a delicately balanced process, regulated by external signals or the internal genetic program of an individual cell. In psoriasis, these processes are disturbed and some candidate genes like p53 are suspected of being involved in the pathogenesis of the disease. The p53 protein is essential for the regulation of cell proliferation. The study was performed on 32 patients with psoriasis (24 plaque type, eight guttate type). Biopsy specimens for immunohistochemical determination of p53 protein expression were collected from both the lesional and the nonlesional skin sites that were not exposed to sun in all of the patients (n = 32). Taking the ultraviolet (UV) exposure of the skin into consideration, a third skin sample was taken from each patient (n = 7) who had lesions on the sun-exposed areas. Immunohistochemical assessment of p53 expression in skin was determined as p53 protein expression per 1000 cells (keratinocytes). The statistical analysis revealed that the expressions of p53 per 1000 cells were higher in non-sun-exposed lesional skin than the non-sun-exposed nonlesional skin, also in plaque-type psoriasis than guttate-type psoriasis (P = 0.000, P = 0.046, P = 0.037, respectively). There was a positive correlation between the p53 expression in non-sun-exposed lesional skin versus expression in sun-exposed lesional skin (cubic centimeters = 0.811, P = 0.027). Our results show a stronger association of elevated p53 expression with chronic rather than acute inflammatory psoriasis. This may indicate a mechanistic difference between plaque-type and guttate psoriasis. Alternatively, this could reflect a chronological course as the disease transitions from an acute to a chronic phase.
银屑病是一种常见的炎症性和增殖性皮肤病，其特征为角质形成细胞过度增殖。银屑病的发病机制尚未明确。细胞生长的控制是一个精细平衡的过程，受外部信号或单个细胞的内部遗传程序调节。在银屑病中，这些过程受到干扰，一些候选基因如p53被怀疑参与了该疾病的发病机制。p53蛋白对于细胞增殖的调节至关重要。该研究对32例银屑病患者（24例斑块型，8例点滴型）进行。从所有患者（n = 32）未暴露于阳光的皮损部位和非皮损部位采集活检标本，用于免疫组织化学测定p53蛋白表达。考虑到皮肤的紫外线（UV）暴露情况，从每个在阳光暴露部位有皮损的患者（n = 7）身上采集第三份皮肤样本。皮肤中p53表达的免疫组织化学评估以每1000个细胞（角质形成细胞）中的p53蛋白表达来确定。统计分析显示，每1000个细胞中p53的表达在未暴露于阳光的皮损皮肤中高于未暴露于阳光的非皮损皮肤，在斑块型银屑病中也高于点滴型银屑病（分别为P = 0.000、P = 0.046、P = 0.037）。未暴露于阳光的皮损皮肤中的p53表达与暴露于阳光的皮损皮肤中的表达之间存在正相关（立方厘米 = 0.811，P = 0.027）。我们的结果表明，p53表达升高与慢性而非急性炎症性银屑病的关联更强。这可能表明斑块型和点滴型银屑病之间存在机制差异。或者，这可能反映了疾病从急性期向慢性期转变的时间进程。
