Impact of the Gly573Ser Substitution in TRPV3 on the Development of Allergic and Pruritic Dermatitis in Mice

We reported that the Gly573Ser substitution in transient receptor potential vanilloid 3 (TRPV3) led to increased ion channel activity in keratinocytes and caused spontaneous hairlessness in DS-Nh mice. DS-Nh mice also develop allergic and pruritic dermatitis. As the hairless and dermatitis phenotype...

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Bibliographic Details
Published in:Journal of investigative dermatology 2009-03, Vol.129 (3), p.714-722
Main Authors: Yoshioka, Takeshi, Imura, Kinichi, Asakawa, Makoto, Suzuki, Minoru, Oshima, Itsuki, Hirasawa, Tsutomu, Sakata, Tsuneaki, Horikawa, Tatsuya, Arimura, Akinori
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Dermatitis - metabolism
Dermatology
Glycine - chemistry
Hypersensitivity - metabolism
Immunoglobulin E - metabolism
Ligands
Medical sciences
Mice
Mice, Inbred C57BL
Mice, Transgenic
Phenotype
Promoter Regions, Genetic
Pruritus - metabolism
Serine - chemistry
Skin involvement in other diseases. Miscellaneous. General aspects
TRPV Cation Channels - genetics
TRPV Cation Channels - metabolism
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Summary:We reported that the Gly573Ser substitution in transient receptor potential vanilloid 3 (TRPV3) led to increased ion channel activity in keratinocytes and caused spontaneous hairlessness in DS-Nh mice. DS-Nh mice also develop allergic and pruritic dermatitis. As the hairless and dermatitis phenotypes were both inherited in an autosomal dominant fashion and could not be segregated from each other, we speculated that TRPV3Gly573Ser might be responsible for the dermatitis. Here, we constructed TRPV3Gly573Ser transgenic mice, with a putative promoter sequence in the 5′ region of TRPV3, to investigate the involvement of TRPV3 in the development of specific types of dermatitis. These transgenic mice spontaneously developed dermatitis, whereas wild-type mice did not display this phenotype when maintained under the same conditions. Histological and serological analyses were carried out to better understand the clinical features of TRPV3Gly573Ser transgenic mice. A physiological study revealed that TRPV3Gly573Ser induced a higher nerve growth factor response to heat. Finally, C57BL-Nh mice were used to investigate the penetrance of the TRPV3Gly573Ser gene for dermatitis. Interestingly, C57BL-Nh mice developed spontaneous scratching behavior, separately from the development of dermatitis. We propose that TRPV3Gly573Ser is a cause of pruritus and/or dermatitis associated with scratching, and suggest that TRPV3 may represent a therapeutic target in pruritic dermatitis.
ISSN:0022-202X
1523-1747
DOI:10.1038/jid.2008.245