The function and mechanism of Transgelin that expresses in injured glomerular epithelial cells.
| Project/Area Number |
22590882
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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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 | Niigata University |
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Principal Investigator |
SAKATSUME Minoru 新潟大学, 医歯(薬)学総合研究科, 非常勤講師 (70334662)
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| Co-Investigator(Kenkyū-buntansha) |
KURODA Takeshi 新潟大学, 保健管理センター, 准教授 (00372475)
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| Research Collaborator |
酒巻 裕一 , 大学院生
猪俣 繁 , 大学院生
王 興智 , 大学院生
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2012: ¥390,000 (Direct Cost: ¥300,000、Indirect Cost: ¥90,000)
Fiscal Year 2011: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2010: ¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
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| Keywords | 腎組織障害 / トランスゲリン / SM22α / 糸球体障害 / 尿細管間質障害 / 腎臓内科学 / 糸球体上皮障害 / Transgelin / バイオマーカー |
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| Research Abstract |
Transgelin has been revealed to express in injured glomerukar epithelial cells and interstitial cells of both rat and human. It is located in the area of foot process effacement and represents the podocyte injury in glomeruli. The expression is specific for renal cell injury. The extent of its positivity in glomerular or tubulointerstitial area is the determinant of the amount of proteinuria or the deterioration of creatinine clearance (Ccr), respectively. The mechanism of its expression largely depends on the signal transduction of TGFβ.
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Report
(4 results)
Research Products
(13 results)
