Quantitative fluorescence in situ hybridization measurement of telomere length in skin with/without sun exposure or actinic keratosis

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• 作者：Hiroyuki Ikeda ; Junko Aida ; Atsushi Hatamochi ; Yoichiro Hamasaki ; Naotaka Izumiyama-Shimomura ; Ken-ichi Nakamura ; Naoshi Ishikawa ; Steven S. Poon ; Mutsunori Fujiwara ; Ken-ichiro Tomita ; Naoki Hiraishi ; Mie Kuroiwa ; Masaaki Matsuura ; Yukihiro Sanada ; Youichi Kawano ; Tomio Arai ; Kaiyo Takubo
• 关键词：Actinic keratosis ; Telomere ; Aging ; Photoaging ; Epidermis ; Q-FISH ; Dermis
• 刊名：Human Pathology
• 出版年：March, 2014
• 年：2014
• 卷：45
• 期：3
• 页码：473-480
• 全文大小：1881 K

文摘

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Summary

Chromosomal and genomic instability due to telomere dysfunction is known to play an important role in carcinogenesis. To study telomere shortening in the epidermis surrounding actinic keratosis, we measured telomere lengths of basal, parabasal, and suprabasal cells in epidermis with actinic keratosis (actinic keratosis group, n = 18) and without actinic keratosis (sun-protected, n = 15, and sun-exposed, n = 13 groups) and in actinic keratosis itself as well as in dermal fibroblasts in the 3 groups, using quantitative fluorescence in situ hybridization. Among the 3 cell types, telomeres of basal cells were not always the longest, suggesting that tissue stem cells are not necessarily located among basal cells. Telomeres of basal cells in the sun-exposed group were shorter than those in the sun-protected group. Telomeres in the background of actinic keratosis and in actinic keratosis itself and those of fibroblasts in actinic keratosis were significantly shorter than those in the controls. Our findings demonstrate that sun exposure induces telomere shortening and that actinic keratosis arises from epidermis with shorter telomeres despite the absence of any histologic atypia.