| Project/Area Number |
26670431
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Kidney internal medicine
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| Research Institution | Kyoto University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
SHIRATA NARITOSHI 京都大学, 大学院医学研究科, 客員研究員 (00726200)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2016: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | ポドサイト / 糸球体硬化 / Dendrin / MAGI-2 / Podocin / SNX-9 / スリット膜 / 足突起 / SNX9 / 蛋白分解 |
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| Outline of Final Research Achievements |
It has recently become clear that initial glomerular injury affects glomerular podocytes, making them important target cells for progression of chronic kidney disease (CKD). Podocyte injury may cause podocyte detachment from the GBM, which leads to glomerulosclerosis. We have reported that dendrin translocates to the nucleus in injured podocytes, promoting podocyte apoptosis. Moreover, nuclear translocation of dendrin was also found in human kidney biopsy specimens from patients with glomerular diseases characterized by podocyte loss and glomerulosclerosis. We found that MAGI-2 is necessary for inhibiting dendrin nuclear translocation under physiological conditions. We have demonstrated the endocytic translocation of podocin to the subcellular area in injured podocytes. we identified SNX9 as a facilitator of podocin endocytosis in severe podocyte injury and demonstrated the expression of SNX9 in the podocytes of irreversible glomerular disease.
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