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5‐Bromo‐2′‐deoxyuridine induced effluvium via p53‐mediated CD 326‐positive keratinocyte apoptosis in C57 BL /6 mice
Author(s) -
Uh KyungJun,
Hwang WooSung,
Bae JiHyun,
Jang DaEun,
Yeom SuCheong
Publication year - 2017
Publication title -
the journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.9
H-Index - 65
eISSN - 1346-8138
pISSN - 0385-2407
DOI - 10.1111/1346-8138.13547
Subject(s) - hair loss , apoptosis , hair follicle , flow cytometry , bromodeoxyuridine , keratinocyte , biology , hair cycle , immunohistochemistry , endocrinology , immunology , medicine , in vitro , biochemistry , genetics
Anagen effluvium develops because of disturbances in the hair follicle cycle, leading to acute and severe hair loss in humans. The objective of this study was to establish a mouse model of anagen effluvium by 5‐bromo‐2′‐deoxyuridine (BrdU) treatment, and evaluate the pathological changes and underlying mechanisms. We treated 9–10‐day‐old pups and 3–7‐week‐old C57 BL /6 mice with BrdU. After successfully inducing hair loss in the neonatal pups, microscopic, immunohistochemical and flow cytometry analyses were conducted. BrdU induced early onset alopecia in neonates and caused epidermal thickening and hair shaft breakage. BrdU appeared to incorporate the CD 326‐positive keratinocyte layer and induced p53‐related apoptosis. Keratinocyte apoptosis caused immune cell infiltration in the dermal region; M2 macrophages and neutrophils were dominant. The BrdU‐induced hair loss was dose‐dependent, and alopecia was visible at a dose range of 25–200 μg/g bodyweight. The BrdU‐induced anagen effluvium mouse model is novel and easily established by administrating four simple BrdU injections to pups; these mice showed synchronized onset of alopecia symptoms with little individual variation. Moreover, this model showed an alopecia phenotype similar to that of human anagen effluvium with acute, severe and widespread hair loss.