2019 Fiscal Year Final Research Report

Generation of salivary gland-specific injury model mouse and elucidation of repair mechanism by EGFR2 / MUC1 pathway

Research Project

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Project/Area Number	17K11633
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Multi-year Fund
Section	一般
Research Field	Morphological basic dentistry
Research Institution	Tsurumi University
Principal Investigator	MATSUMOTO Naoyuki 鶴見大学, 歯学部, 准教授 (20386080)
Co-Investigator(Kenkyū-buntansha)	梁洪淵鶴見大学, 歯学部, 講師 (10298268) 内田仁司鶴見大学, 歯学部, 学内講師 (20736996) 井上裕子日本薬科大学, 薬学部, 教授 (50367306) 中山亮子鶴見大学, 歯学部, 助教 (50749843) 斎藤一郎鶴見大学, 歯学部, 教授 (60147634)
Project Period (FY)	2017-04-01 – 2020-03-31
Keywords	唾液腺 / 組織傷害 / 遺伝子改変マウス
Outline of Final Research Achievements	It is difficult to accurately evaluate the effect of regenerative therapy in conventional mouse models of salivary gland injury, because various organs other than salivary glands are injured. Therefore, an animal model of salivary gland injury has been required. In this study, we established a salivary gland-specific injury model mouse by gene modification using the Toxin receptor-mediated cell knockout (TRECK) as a model of salivary gland injury. Diphtheria toxin (DT) was injected into the transgenic mouse, and the amount of pilocarpine-stimulated salivary secretion was measured. As a result, it decreased to about 55% 168 hours after the administration of DT. Furthermore, histological examination revealed an increase of TUNEL-positive apoptotic cell as compared with the wild type.
Free Research Field	病理学
Academic Significance and Societal Importance of the Research Achievements	本研究では唾液腺局所に発現するプロモーターによる遺伝子改変マウスを作出し、唾液腺特異的に組織が障害されることを確認した。この遺伝子改変マウスはこれまでにない病態モデルとなり、唾液腺障害に起因する唾液分泌障害のメカニズムの解析や、唾液腺組織再生治療の開発の為に、唾液腺を特異的に障害するモデル動物の開発が極めて有効な研究戦略となると考えられる。今後、この遺伝子改変マウスを利用して組織傷害や再生の詳細を検討する。