Abnormal keratin expression pattern in prurigo nodularis epidermis

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 th...

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Main Authors: L. L. Yang, B. Jiang, S. H. Chen, H. Y. Liu, T. T. Chen, L. H. Huang, M. Yang, J. Ding, J. J. He, J. J. Li, B. Yu
Format: Article
Language:English
Published: Wiley 2022-03-01
Series:Skin Health and Disease
Online Access:https://doi.org/10.1002/ski2.75
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author L. L. Yang
B. Jiang
S. H. Chen
H. Y. Liu
T. T. Chen
L. H. Huang
M. Yang
J. Ding
J. J. He
J. J. Li
B. Yu
author_facet L. L. Yang
B. Jiang
S. H. Chen
H. Y. Liu
T. T. Chen
L. H. Huang
M. Yang
J. Ding
J. J. He
J. J. Li
B. Yu
author_sort L. L. Yang
collection DOAJ
description 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.
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spelling doaj.art-81ab0631fee2467ea0d457b997059b672022-12-22T02:48:13ZengWileySkin Health and Disease2690-442X2022-03-0121n/an/a10.1002/ski2.75Abnormal keratin expression pattern in prurigo nodularis epidermisL. L. Yang0B. Jiang1S. H. Chen2H. Y. Liu3T. T. Chen4L. H. Huang5M. Yang6J. Ding7J. J. He8J. J. Li9B. Yu10Department of Dermatology Peking University Shenzhen Hospital Shenzhen Guangdong ChinaDepartment of Dermatology Peking University Shenzhen Hospital Shenzhen Guangdong ChinaDepartment of Dermatology Peking University Shenzhen Hospital Shenzhen Guangdong ChinaDepartment of Dermatology Peking University Shenzhen Hospital Shenzhen Guangdong ChinaDepartment of Dermatology Affiliated Shenzhen Longhua People's Hospital of Southern Medical University Shenzhen Guangdong ChinaGuanghe Hui Shenzhen Guangdong ChinaNational Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital & Shenzhen Hospital Chinese Academy of Medical Sciences and Peking Union Medical College Shenzhen Guangdong ChinaDepartment of Dermatology Shenzhen Baoan Maternal and Child Health Hospital Shenzhen Guangdong ChinaDepartment of Plastic and Cosmetic Surgery Peking University Shenzhen Hospital Shenzhen Guangzhou ChinaDepartment of Dermatology Peking University Shenzhen Hospital Shenzhen Guangdong ChinaDepartment of Dermatology Peking University Shenzhen Hospital Shenzhen Guangdong ChinaAbstract 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.https://doi.org/10.1002/ski2.75
spellingShingle L. L. Yang
B. Jiang
S. H. Chen
H. Y. Liu
T. T. Chen
L. H. Huang
M. Yang
J. Ding
J. J. He
J. J. Li
B. Yu
Abnormal keratin expression pattern in prurigo nodularis epidermis
Skin Health and Disease
title Abnormal keratin expression pattern in prurigo nodularis epidermis
title_full Abnormal keratin expression pattern in prurigo nodularis epidermis
title_fullStr Abnormal keratin expression pattern in prurigo nodularis epidermis
title_full_unstemmed Abnormal keratin expression pattern in prurigo nodularis epidermis
title_short Abnormal keratin expression pattern in prurigo nodularis epidermis
title_sort abnormal keratin expression pattern in prurigo nodularis epidermis
url https://doi.org/10.1002/ski2.75
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