| Project/Area Number |
22249033
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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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 | Tokai University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
ICHIKAWA Iekuni 東海大学, 医学部, 客員教授 (80317768)
NIIMURA Fumio 東海大学, 医学部・小児科学, 准教授 (30282750)
NISHIYAMA Akira 香川大学, 医学部・薬理学, 教授 (10325334)
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| Research Collaborator |
CAMPBELL Duncan J. St. Vincent's Institute of Medical Research, Australia, Professor
PASTAN Ira National Institutes of Health, Bethesda, Maryland, Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, Professor
柳田 素子 京都大学医学部, 大学院医学研究科, 教授
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| Project Period (FY) |
2010-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥46,670,000 (Direct Cost: ¥35,900,000、Indirect Cost: ¥10,770,000)
Fiscal Year 2014: ¥9,100,000 (Direct Cost: ¥7,000,000、Indirect Cost: ¥2,100,000)
Fiscal Year 2013: ¥9,100,000 (Direct Cost: ¥7,000,000、Indirect Cost: ¥2,100,000)
Fiscal Year 2012: ¥9,100,000 (Direct Cost: ¥7,000,000、Indirect Cost: ¥2,100,000)
Fiscal Year 2011: ¥9,100,000 (Direct Cost: ¥7,000,000、Indirect Cost: ¥2,100,000)
Fiscal Year 2010: ¥10,270,000 (Direct Cost: ¥7,900,000、Indirect Cost: ¥2,370,000)
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| Keywords | AngiotensinⅡ / Angiotensinogen / ポドサイト / 慢性腎不全 / ノックアウトマウス / Magalin / 糸球体硬化症 / ネフローゼ症候群 / 腎間質線維化 / AngiotensinII / Megalin / megalin / Angiotensin II |
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| Outline of Final Research Achievements |
In chronic kidney diseases caused by diabetes or nephritis, the key event is injury in a unique type of cells, called podocytes. Podocyte injury triggers progressive deterioration of kidney function. In the present study, we established a method to comprehensively analyze gene expression selectively in podocytes. We also revealed the mechanism underlining induction of angiotensin II within the kidney. Angiotensin II is the most potent blood pressure-raising hormone, and also may further worsen kidney injury. Podocyte injury causes leakage of angiotensinogen, the precursor protein of angiotensin II, which is reabsorbed by kidney cells, and then converted to angiotensin II. This finding provides an insight into mechanism underlining progressive worsening of kidney diseases.
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