Mechanisms regulating the maintenance of nephron progenitors
| Project/Area Number |
23390228
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Kidney internal medicine
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| Research Institution | Kumamoto University |
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Principal Investigator |
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| Project Period (FY) |
2011-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥19,500,000 (Direct Cost: ¥15,000,000、Indirect Cost: ¥4,500,000)
Fiscal Year 2013: ¥6,110,000 (Direct Cost: ¥4,700,000、Indirect Cost: ¥1,410,000)
Fiscal Year 2012: ¥6,110,000 (Direct Cost: ¥4,700,000、Indirect Cost: ¥1,410,000)
Fiscal Year 2011: ¥7,280,000 (Direct Cost: ¥5,600,000、Indirect Cost: ¥1,680,000)
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| Keywords | 腎臓学 / 腎臓発生 / ネフロン前駆細胞 / 発生・分化 / 幹細胞 |
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| Research Abstract |
The adult kidney never regenerates, but the embryonic kidney contains nephron progenitors. The purpose of this project was to reveal molecular mechanisms underlying the maintenance of the embryonic nephron progenitors. We generated progenitor-specific and drug-inducible Sall1 mutant mice, and found that nephron progenitors were rapidly depleted upon Sall1 deletion. We identified the direct downstream targets of Sall1 and found that Sall1 functions as a positive regulator in the progenitors, while repressing aberrant gene expression in differentiating nascent nephrons. We are currently trying to establish a method to self-renew the progenitors, by utilizing the obtained information. If successful, it would serve as a basis toward kidney regeneration, because the nephron progenitors disappear shortly after birth in a normal condition.
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Report
(4 results)
Research Products
(18 results)
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[Journal Article] Sall1 maintains nephron progenitors and nascent nephrons by acting as both an activator and a repressor2014
Author(s)
S. Kanda, T. Ohmori, A. Taguchi, K. Kudo, T. Horiuchi, Y. Sato, S. Hino, Y. Suzuki, M. Sander, S. Sugano, M. Nakao, and R. Nishinakamura.
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Journal Title
J. Am. Soc. Nephrol.
Volume: 25
Issue: 11
Pages: 2584-2595
DOI
Related Report
Peer Reviewed / Open Access
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