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2021 Fiscal Year Final Research Report

Identification of signaling pathways regulating follicular function by follicular Tg to elucidate the pathogenesis of thyroid diseases

Research Project

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Project/Area Number 19K07875
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Review Section Basic Section 52010:General internal medicine-related
Research InstitutionTeikyo University

Principal Investigator

Suzuki Koichi  帝京大学, 医療技術学部, 教授 (20206478)

Co-Investigator(Kenkyū-buntansha) 山中 大介  東京大学, 大学院農学生命科学研究科(農学部), 特任助教 (10553266)
川島 晃  帝京大学, 医療技術学部, 研究員 (60624913)
Project Period (FY) 2019-04-01 – 2022-03-31
Keywords甲状腺 / サイログロブリン / 細胞内シグナル伝達
Outline of Final Research Achievements

Thyroglobulin, a precursor of thyroid hormone accumulated in the thyroid follicles, completely reverse the ability of TSH to induce thyroid hormone synthesis by an autocrine negative-feedback action. We have shown that Tg does not directly inhibit signaling downstream of the TSH receptor, but regulates the expression of genes required for hormone synthesis through other pathways. In addition, we showed that the expression level and membrane localization of novel apical iodide transporter SLC26A7 are down-regulated by follicular concentration of Tg, suggesting that the function of individual follicles is tightly regulated by the level of Tg accumulated in the follicule.

Free Research Field

内分泌学、分子細胞生物学、病理学

Academic Significance and Societal Importance of the Research Achievements

甲状腺濾胞内に蓄積するサイログロブリンは、下垂体から分泌される甲状腺刺激ホルモン(TSH)の作用を強力に阻害する。本研究によって、その作用は予測されたTSH受容体下流のシグナルを直接阻害するのでは無く、未知の経路を介することが明らかとなった。Tg作用の異常は甲状腺機能異常に直結すると考えられることから、そのような異常の新たな診断法や治療法の開発に展開できることが期待された。

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Published: 2023-01-30  

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