| Project/Area Number |
25460275
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
General anatomy (including histology/embryology)
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| Research Institution | Jichi Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
AZUMA Morio 自治医科大学, 医学部, 助教 (90709643)
YASHIRO Takashi 自治医科大学, 医学部, 教授 (80119859)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 下垂体前葉 / 細胞分化 / カドヘリン / Notch / 下垂体 / cadherin / 前駆細胞 / 腺下垂体 / 細胞接着 / 細胞間相互作用 / 細胞接着因子 / Notchシグナル |
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| Outline of Final Research Achievements |
The anterior pituitary is composed of types of hormone-producing cells. Progenitor cells that can differentiate into the types of cells were reported to be maintained in adult tissue. Differentiation is regulated by humoral factors, however, the mechanism to maintain progenitor cells was not understood. We previously showed Notch signaling, a regulator of progenitor cells in many organs, is activated in particular cell aggregates in rat pituitary. In this study, immunohistochemistry revealed a close relationship between Notch signaling molecules and cell adhesion molecule E-cadherin. Expression of the target HES1 decreased by E-cadherin inhibition in primary culture. Notch receptor and ligand were always co-localized within cells, suggesting homologous cells have reciprocal effects. We are further analyzing genes regulated by Notch signaling. The present study suggests that E-cadherin-mediated cell attachment is responsible for maintenance of progenitor cells through Notch signaling.
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