アクティブボード・２００９年　６月
　　　　　・・・・・２００９年　６月　４日更新・・・・・

研究発表を行った学会；
・The Kumamoto University Global COE International Joint Symposium on Cell Fate Regulation Research: Molecular Basis and Therapeutic Potentials.
　２００９年　４月　９日〜１０日（熊本）

タイトル；Increased scratching behavior and susceptibility to dermatitis in mite-infected ΔF508 CFTR mice.
　
発表者；　水之江　翔太　氏
　　　（熊本大学　大学院医学薬学研究部　遺伝子機能応用学分野）
Abstract；
　The cystic fibrosis transmembrane conductance regulator (CFTR), in which a mutation causes cystic fibrosis, is a polytopic integral membrane protein that mediates transepithelial chloride transport across epithelial cells in airways, pancreas, intestines, sweat glands and other tissues. In addition, CFTR also regulates various molecules such as epithelial sodium channel (ENaC) and aquaporin 3 (AQP3). CFTR is an extremely important molecule for the maintenance of homeostasis and plays a role as universal regulator of a variety of cellular and membrane functions. Thus, CFTR dysfunction could cause abnormalities in tissues such as the respiratory tract, gastrointestinal tract and sweat glands. Recent report shows that CFTR is expressed in human epidermis. However the function and role of CFTR in the skin is unknown. It is also unclear whether CFTR mutation has adverse effect specifically in the epidermis. Here, we assessed the effect of CFTR dysfunction on the development of cutaneous symptoms (itch, skin fibrosis) using ΔF508 CFTR mutant mice (CFTRΔF508/ΔF508). When exposed to rodent mite (Myobia musculi), but not when they were housed in mite-free environment, the CFTRΔF508/ΔF508 mice displayed an increased number of scratching count and skin fibrosis with an accompanying increase in the level of nerve growth factor (NGF) and protein gene product 9.5 (PGP9.5). On the other hand, CFTR+/ΔF508 and CFTRΔF508/ΔF508 mice exposed to mite did not display abnormal scratching behavior and skin fibrosis. These data suggest that homozygous ΔF508 CFTR does not trigger spontaneous dermatosis but may affect the response to skin allergen.