A novel hairless mouse model on an atopic dermatitis-prone genetic background generated by receptor-mediated transgenesis |
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Authors: | Toyoyuki Takada Hiroshi Shitara Kunie Matsuoka Erika Kojima Rie Ishii Yoshiaki Kikkawa Choji Taya Hajime Karasuyama Kenji Kohno Hiromichi Yonekawa |
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Institution: | Department of Laboratory Animal Science, The Tokyo Metropolitan Institute of Medical Science (Rinshoken), 3-18-22, Honkomagome, Bunkyo-ku, Tokyo 113-8613, Japan. |
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Abstract: | Current mouse models for atopic dermatitis (AD) have a serious drawback, being the existence of dense hair on the body. Thus,
a hairless animal model on an AD-prone genetic background will be a powerful tool to investigate the basis of and therapy
for this complex disease. We applied the Toxin Receptor-mediated Cell Knockout (TRECK) method to generate a hairless transgenic
(Tg) mice on the NC/Nga background, an AD-prone inbred strain. A minigene with the mouse Keratin71 (Krt71) promoter and human diphtheria toxin receptor, which intrinsically functions as the heparin-binding EGF-like growth factor,
was introduced into the pronucleus of NC/Nga oocytes. Unexpectedly NCN24, one NC/Nga Tg line, showed a dominant hairless phenotype
without diphtheria toxin administration. Furthermore, the atopic dermatitis-like predisposition and IgE elevation was observed
in both NCN24 and the NC/Nga wildtype strain. NCN24 mice, which we have newly developed, will be useful to assess drugs for
AD therapy, being able to monitor skin inflammation without shaving.
Electronic supplementary material The online version of this article (doi:) contains supplementary material, which is available to authorized users. |
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Keywords: | Receptor-mediated transgenesis NC/Nga inbred strain Hairless mouse model Atopy |
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