Abstract Prurigo nodularis (PN) is a highly pruritic chronic inflammatory dermatosis with unknown pathogenesis. It is characterized by the existence of many hyperkeratotic, erosive papules and nodules, and the development of lesions may be associated with hyperproliferation and aberrant differentiation of keratinocytes. Keratin 17 (K17) is overexpressed selectively in human proliferative skin diseases, promoting keratinocyte proliferation not found in normal epidermis. In this study, we investigated the mRNA levels and protein levels of K17 in lesional and perilesional skin using quantitative real-time polymerase chain reaction and western blot. We demonstrate that K17 is induced in lesional and perilesional skin in PN. The mRNA expression level of K17 was upregulated in PN lesions (P < 0.01), with multifold changes in the PN lesion (normalized to glyceraldehyde-3-phosphate dehydrogenase as the housekeeping gene) showing a median positive correlation with PRUNOSI (P < 0.05). The protein level of K17 was also markedly increased in PN lesions (P < 0.01). In conclusion, K17 is highly induced in PN lesions, which may contribute to the proliferation of keratinocytes and the pathogenesis of PN. Graphical Abstract

中文翻译：

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角蛋白 17 在结节性痒疹病变中被诱导

摘要 结节性痒疹（PN）是一种高度瘙痒的慢性炎症性皮肤病，发病机制不明。它的特点是存在许多角化过度、糜烂性丘疹和结节，病变的发展可能与角质形成细胞的过度增殖和异常分化有关。角蛋白 17 (K17) 在人类增殖性皮肤病中选择性过度表达，促进正常表皮中未发现的角质形成细胞增殖。在这项研究中，我们使用定量实时聚合酶链反应和蛋白质印迹研究了病灶和病灶周围皮肤中 K17 的 mRNA 水平和蛋白质水平。我们证明 K17 在 PN 的病灶和病灶周围皮肤中被诱导。K17 mRNA 表达水平在 PN 病变中上调（P < 0.01），PN 病变的多倍变化（标准化为作为管家基因的 3-磷酸甘油醛脱氢酶）显示与 PRUNOSI 的中位数正相关（P < 0.05）。K17蛋白水平在PN病变中也显着升高（P < 0.01）。总之，K17在PN病变中高度诱导，这可能有助于角质形成细胞的增殖和PN的发病机制。图形概要