Elucidation of the mechanism of maintaining homeostasis through crosstalk between pancreatic endocrine cells
Project/Area Number |
18K08501
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Review Section |
Basic Section 54040:Metabolism and endocrinology-related
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Research Institution | Gunma University |
Principal Investigator |
Nakagawa Yuko 群馬大学, 生体調節研究所, 助教 (90422500)
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Project Period (FY) |
2018-04-01 – 2021-03-31
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Project Status |
Completed (Fiscal Year 2020)
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Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2020: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2019: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2018: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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Keywords | 膵内分泌細胞 / 膵島 / PP細胞 / グルカゴン |
Outline of Final Research Achievements |
We found that PP cell hyperplasia and PP+ GCG+ double positive cells were induced in mice lacking the proglucagon gene. We investigated which hormone the proglucagon gene encodes, and found that glucagon action deficiency induced PP cell hyperplasia and PP+ GCG+ double positive cells. Next, we examined which tissues are involved in this phenotype and found that glucagon action deficiency in the liver is involved. These results suggest that glucagon action in the liver may be involved in the regulation of PP cell proliferation and maintenance of PP cell or α cell fate.
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Academic Significance and Societal Importance of the Research Achievements |
本研究の目的は、プログルカゴン遺伝子欠損マウスにおいて認められたPP細胞の過形成および多重ホルモン産生細胞の発現誘導のメカニズムを解明することである。この結果より生物の普遍的な問いである細胞増殖と細胞運命の制御機構の未知なる領域に迫ろうとするもので、きわめて高い新規性をもつ研究である。また我々は細胞系譜追跡用マウスおよびその他の遺伝子改変マウスを用いた検討より、従来見過ごされていたPP細胞の新しい生理的機能を明らかにしつつある。本研究により、今まで未開拓であったPP細胞の生物学および膵内分泌細胞間のクロストークを介した恒常性維持のメカニズムが明らかになることが期待される
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Report
(4 results)
Research Products
(5 results)
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[Journal Article] Development of monoclonal mouse antibodies that specifically recognize pancreatic polypeptide.2019
Author(s)
Hara A, Nakagawa Y, Nakao K, Tamaki M, Ikemoto T, Shimada M, Matsuhisa M, Mizukami H, Maruyama N, Watada H, Fujitani Y.
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Journal Title
Endocr. J.
Volume: EJ18-0441
Pages: 1-10
NAID
Related Report
Peer Reviewed
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