ALTERED [I-125] EPIDERMAL GROWTH-FACTOR BINDING AND RECEPTOR DISTRIBUTION IN PSORIASIS
ALTERED [I-125] EPIDERMAL GROWTH-FACTOR BINDING AND RECEPTOR DISTRIBUTION IN PSORIASIS
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DOI：
10.1111/1523-1747.ep12285389
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发表时间：
1986-03-01
影响因子：
6.5
通讯作者：
KING, LE
中科院分区：
文献类型：
--
作者：
NANNEY, LB;STOSCHECK, CM;KING, LE
表皮生长因子（epidermal growth factor， EGF）通过与特异性受体的结合来促进人表皮的生长和分化。在寻常型银屑病等增生性疾病中，EGF受体是否主要介导细胞分裂或分化尚不清楚。为了研究银屑病的发病机制，采用放射自显影、免疫组织化学和生化方法检测正常、未受累和受累银屑病皮肤的4 mm2穿孔活检标本中EGF受体的含量。使用放射自显影和免疫组织化学方法，发现与正常表皮和银屑病皮肤的表皮上层相比，基底角化细胞含有最多的EGF结合位点和免疫反应受体。正常表皮和银屑病表皮在这一层未观察到EGF受体的差异。在表皮上层，银屑病皮肤的EGF结合能力比正常薄皮或厚皮增加2倍。生化方法表明，与相同厚度的正常表皮相比，银屑病表皮中的[125I]EGF结合在蛋白质基础上增加。表皮生长因子可增加皮肤中表皮生长因子受体的磷酸化。未分裂棘层和角化不全角质层中保留的EGF受体可能反映了活动性银屑病病变中发生的不完全异常分化。另外，保留的EGF受体可能在抑制基底上层的细胞分化中起直接作用。
Stimulation of growth and differentiation of human epidermis by epidermal growth factor (EGF) is mediated by its binding to specific receptors. Whether EGF receptors primarily mediate cell division or differentiation in hyperproliferative disease such as psoriasis vulgaris is unclear. To study the pathogenesis of psoriasis, 4-mm2 punch biopsy specimens of normal, uninvolved, and involved psoriatic skin were assayed for EGF receptors by autoradiographic, immunohistochemical, and biochemical methods. Using autoradiographic and immunohistochemical methods, basal keratinocytes were found to contain the greatest number of EGF binding sites and immunoreactive receptors as compared to the upperlayers of the epidermis in both normal epidermis and psoriatic skin. No EGF receptor differences between normal and psoriatic epidermis were observed in this layer. In the upper layers of the epidermis, a 2-fold increase in EGF binding capacity was observed in psoriatic skin as compared with normal thin or thick skin. Biochemical methods indicated that [125I]EGF binding was increased in psoriatic epidermis as compared with similar thickness normal epidermis when measured on a protein basis. Epidermal growth factor wasshown to increase phosphorylation of the EGF receptor in skin. EGF receptors retained in the nonmitotic stratum spinosum and parakeratotic stratum corneum may reflect the incomplete abnormal differentiation that occurs in active psoriatic lesions. Alternatively, retained EGF receptors may play a direct role in inhibiting cellular differentiation in the suprabasal layers.