Abstract

Solar lentigo (SL) is characterized by macular lesions exhibiting epidermal hyperplasia combined with hyperpigmentation along with irregular elongation of epidermal rete ridges. This study was conducted to assess the melanosomes in keratinocytes and the activation state of melanocytes in SL lesions on the backs of healthy Japanese individuals. Large melanosome complexes were increased in keratinocytes, and tyrosinase (TYR) activity, as well as immunohistochemical reactivity, for premelanosome protein 17 (Pmel17) in the SL lesions increased compared to the perilesions of five volunteers with SL. The levels of TYR, microphthalmia-associated transcription factor (MITF), and KIT mRNAs, but not stem cell factor (SCF) mRNA, were significantly increased in the SL lesions compared to the perilesions for all samples. Additionally, keratinocytes became immunoreactive to KIT in the rete ridge hyperplasia and basal layers of the SL lesions. These results suggested that the hyperpigmentation of SL arises primarily from increased melanogenesis of existing melanocytes in the basal layer of the epidermis, as well as increased large melanosome complexes in keratinocytes, which probably arise via an increase in KIT signaling in the epidermis.

Highlights

  • Solar lentigo (SL), known as a sun-induced freckle or senile lentigo, is a hyperpigmentation that occurs increasingly with age in sun-exposed areas, such as the face, forearms, back, and the dorsal sides of hands

  • We focus on the melanosomal complex in keratinocytes and the activation state of melanocytes in the epidermis of SL lesions, as well as perilesional normal skin biopsied from five volunteers

  • Most authors agree that there is an increase of melanin in the basal layer of the epidermis with irregular elongation of epidermal rete ridges, as well as an increase in large melanosome complexes in basal keratinocytes of the epidermis [4,5,6,8,9,10]

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Summary

Introduction

Solar lentigo (SL), known as a sun-induced freckle or senile lentigo, is a hyperpigmentation that occurs increasingly with age in sun-exposed areas, such as the face, forearms, back, and the dorsal sides of hands. It is speculated that chronic exposure to UV radiation is a crucial pathogenic factor for the development of SL.

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