Keratin 17 is induced in prurigo nodularis lesions

Author:

Yang Li-Li1,Huang Hai-Yan2,Chen Zhen-Zhen2,Chen Ran3,Ye Rong2,Zhang Wei4,Yu Bo2

Affiliation:

1. Peking University Shenzhen Hospital, Shenzhen Peking University-The Hong Kong University of Science and Technology Medical Center, Shenzhen, China, No.1120 of Lianhua Road, Futian District, Guangdong Province, 518036, China

2. Peking University Shenzhen Hospital, No. 1120 of Lianhua Road, Futian District, Guangdong Province, 518036, China

3. Department of Breast Surgical Oncology, China National Cancer Center Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China

4. Shenzhen Key Laboratory for Translational Medicine of Dermatology, Shenzhen Peking University-The Hong Kong University of Science and Technology Medical Center, No. 1120 of Lianhua Road, Futian District, Guangdong Province, 518036, China

Abstract

AbstractPrurigo 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.

Publisher

Walter de Gruyter GmbH

Subject

Materials Chemistry,General Chemistry

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