A novel hairless mouse model on an atopic dermatitis-prone genetic background generated by receptor-mediated transgenesis.

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.

• Authors: Toyoyuki Takada, Hiroshi Shitara, Kunie Matsuoka, Erika Kojima, Rie Ishii, Yoshiaki Kikkawa, Choji Taya, Hajime Karasuyama, Kenji Kohno, Hiromichi Yonekawa
• Journal: Transgenic research (Transgenic Res) Vol. 17 Issue 6 Pg. 1155-62 (Dec 2008) ISSN: 0962-8819 [Print] Netherlands
• PMID: 18686008 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• HBEGF protein, human
• Hbegf protein, mouse
• Heparin-binding EGF-like Growth Factor
• Intercellular Signaling Peptides and Proteins
• Immunoglobulin E

Topics

• Animals
• Dermatitis, Atopic (genetics, immunology)
• Disease Models, Animal
• Gene Transfer Techniques
• Heparin-binding EGF-like Growth Factor
• Humans
• Immunoglobulin E (genetics, immunology, metabolism)
• Intercellular Signaling Peptides and Proteins (genetics)
• Mice
• Mice, Hairless
• Mice, Transgenic
• Promoter Regions, Genetic