Immunohistochemical Evaluation and Gene Expression Profiling of Senile Lentigo

BACKGROUND AND OBJECTIVES: Senile lentigines typically appear as dark brown macules on sun-exposed areas. Histologically, they are characterized by hyperpigmentation in the basal layer of the epidermis, combined with elongation of rete ridges. The molecular pathogenesis underlying the initiation and formation of senile lentigines are not completely understood. The histological and immunohistochemical features that characterize facial senile lentigines and their gene expression profiles were investigated. MATERIAL AND METHODS: For routine and immunohistochemical study, formalin-fixed and paraffin-embedded tissue blocks obtained from 20 Korean patients (1 man, 19 women) were used. Immunohistochemical staining of tyrosinase, NKI/beteb, MITF (microphthalmia-associated transcription factor), Ki67, SFRP2 (secreted frizzled-related protein 2), Wnt-5a, p16 and p53 and computer-assisted image analysis were performed. DNA microarray analysis was carried in one female volunteer with both lentigo and melasma. RESULTS: Histological features of senile lentigo of the face were characterized by epidermal hyperpigmentation due to melanocytic proliferation and activation. Epidermal thickness was increased due to increased size of keratinocytes, rather than the number of keratinocytes. In contrast to lentigo occurring elsewhere, facial lentigo in my series showed flattened epidermis rather than lentiginous epidermal hyperplasia in 80% of cases. NKI/beteb and tyrosinase staining suggests melanocytes are constantly activated throughout the evolution of lentigo. Increased expression of p53 in lesion suggests ultraviolet light irradiation is an important factor for epidermal hyperpigmentation. Wnt signaling pathway-associated factors were partially evident in the lesional skin, indicating possible involvement. The severity of senile lentigines could be correlated with the degree of epidermal hyperplasia and categorized, which was further supported by modulations of proliferation and senescence markers. Differentially expressed genes among the normal skin, lentigo and melasma were identified by Affymetrix gene expression analysis, but the results did not match the outcomes derived from immunohistochemistry. CONCLUSIONS: Senile lentigo is a pigmentary disorder of both melanocytes and keratinocytes, controlled by intricate interactions between epidermal and dermal mesenchymal cells.

Author dc:creator

• 신, 재영

Contributors dc:contributor

• 강, 희영
• 대학원 의학과
• 201024243

• lentigo
• immunohistochemistry
• melanocyte
• keratinocyte
• microarray

Language dc:language

ko

Identifier

http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000012356
000000012356

OAI identifier oai:identifier

oai:repository.ajou.ac.kr:201003/7582