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.
Highlights
Prurigo nodularis (PN) is a chronic disorder of the skin characterized by multiple, pruritic, and hyperkeratotic nodules that tend to distribute symmetrically with a predilection on the extensor surfaces of the limbs [1,2]
32% of patients with PN had an atopic background with no signs of active dermatosis, lesions of PN manifested in circumscribed areas, and symmetrical distribution of the extensor surfaces of extremities and trunk
Epidermal keratinocytes may play an important role in the pathogenesis of PN
Summary
Prurigo nodularis (PN) is a chronic disorder of the skin characterized by multiple, pruritic, and hyperkeratotic nodules that tend to distribute symmetrically with a predilection on the extensor surfaces of the limbs [1,2]. Keratinocytes, resident immune cells, and innervating somatosensory nerve fibers interact in direct and indirect ways and are involved in itch [12]. The behavior of keratinocytes in normal and diseased skin is determined mostly by its state of activation or differentiation [14]. Histopathological studies of prurigo nodularis have shown thick epidermis, irregular epidermal hyperplasia, focal parakeratosis, and hypergranulosis in the epidermis [11,15], suggesting that hyperproliferation and aberrant differentiation of keratinocytes may be involved in the formation of PN
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