Abnormal keratin expression pattern in prurigo nodularis epidermis.
Abnormal keratin expression pattern in prurigo nodularis epidermis.
复制标题
结节性痒疹表皮角蛋白异常表达模式
DOI：
10.1002/ski2.75
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发表时间：
2022-03
影响因子：
--
通讯作者：
Yu, B
中科院分区：
文献类型：
--
作者：
Yang, L L;Jiang, B;Chen, S H;Liu, H Y;Chen, T T;Huang, L H;Yang, M;Ding, J;He, J J;Li, J J;Yu, B
摘要背景结节性痒疹（Prurigo结节性痒疹）是一种高度瘙痒性的慢性皮肤病，治疗难度大。PN病变的特点是存在许多角化过度、糜烂性丘疹和结节。然而，PN的发病机制仍不清楚。目的探讨角蛋白在表皮增生中的作用，探讨角蛋白在PN病变皮肤中的表达规律。方法在本研究中，我们招募了24例PN患者和9名健康对照组。免疫组化染色检测细胞K1/K10、K5/K14、K6/K16/K17的表达谱。结果病变皮肤由增厚的棘层组成，棘层内细胞分裂活跃。K5/K14在PN病变表皮中表达上调，染色信号定位于基底层和下基上层。增生相关的K6存在于所有表皮皮损层，尤其是棘层。相比之下，K16仅在基底层和下基上层中检测到，K17在基底层和棘层中检测到。末端差异角蛋白K1/K10上调，在泛表皮中检测到，但在基底层和低基上层中没有。结论角质形成细胞的分化途径与活化的角质细胞表型有关，异常的角质表达可能促进角质形成细胞的增殖，从而导致病变皮肤表皮厚度增加、角化过度和皮肤屏障特性的改变。
Abstract Background Prurigo nodularis (PN) is a highly pruritic, chronic dermatosis and difficult to treat. PN lesions are characterized by existence of many hyperkeratotic, erosive papules and nodules. However, the pathogenesis of PN still remains unelucidated. Aim To clarify the keratin role in the epidermis hyperproliferation, the keratin expression pattern in the PN lesional skin. Methods In this study, we enrolled 24 patients with PN and 9 healthy control volunteers. K1/K10, K5/K14, K6/K16/K17 expression pattern were investigated by using immunohistochemical staining. Results The lesional skin consists of the thickened spinous layers, in which active cell division was found. K5/K14 were upregulated in PN lesional epidermis, the staining signal localized in the basal layer and lower suprabasal layers. Hyperproliferation‐associated K6 was found in all layers of epidermal lesional skin, especially in the spinous layers. In contrast, K16 was only detected in the basal and lower suprabasal layers, K17 was observed in the basal and spinous layers. Terminal differential keratins K1/K10 were upregulated, detected in the pan‐epidermis, but spared in the basal and low suprabasal layers. Conclusion The keratinocytes enter an alternative differentiation pathway, which are responsible for the activated keratinocyte phenotype, abnormal keratins expression potentially contributes to the keratinocytes proliferation, subsequently lead to increased lesional skin epidermis thickness, hyperkeratiosis and alteration of skin barrier properties.