2017 Fiscal Year Final Research Report
Foxc1/2 transcription factors and glomerulosclerosis
| Project/Area Number |
25461234
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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 |
Kidney internal medicine
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| Research Institution | Tokai University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
松阪 泰二 東海大学, 医学部, 教授 (50317749)
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| Co-Investigator(Renkei-kenkyūsha) |
ICHIKAWA Iekuni 東海大学, 医学部, 客員教授 (80317768)
MIYAZAKI Yoichi 東京慈恵会医科大学, 医学部, 教授 (60266690)
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| Research Collaborator |
OHTSUKA Masato 東海大学, 医学部, 准教授 (90372945)
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| Project Period (FY) |
2013-04-01 – 2018-03-31
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| Keywords | 糸球体硬化 / 転写因子 / フォークヘッド / ポドサイト |
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| Outline of Final Research Achievements |
Foxc1 and Foxc2 (Foxc1/2) are transcription factors involved in many biological processes including kidney development. Roles of Foxc1/2 in kidney were examined by conditional knockout mice.
Deletion of Foxc2 from early kidney development by Pax2-Cre resulted in kidney hypoplasia accompanied by glomerular cysts. Mice with an innate podocyte-specific deletion of Foxc1/2 by Nephrin-Cre developed massive proteinuria within 2 weeks after birth. Deletion of Foxc1/2 in adulthood by inducible-Cre resulted in development of massive proteinuria and glomerulosclerosis. Comprehensive gene expression analysis revealed that Foxc1/2 control genes necessary for podocyte function such as podocin and Cxcl12.
These results demonstrate critical roles for Foxc1/2 not only in kidney development but also podocyte maitenance.
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| Free Research Field |
腎臓内科学
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