Podocyte-specific deletion of Rac1 leads to aggravation of renal injury in STZ-induced diabetic mice
Project/Area Number |
26461239
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Kidney internal medicine
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Research Institution | Juntendo University |
Principal Investigator |
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Research Collaborator |
ISHIZAKA Masanori
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Project Period (FY) |
2014-04-01 – 2017-03-31
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Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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Keywords | Rac1 / Diabetic nephropathy / Podocyte / Foot process effacement / Apoptosis / flox/flox / podocin-Cre / streptozotocin / diabetic nephropachy / podocyte / foot process effacement / apoptosis / diabetic nephropathy |
Outline of Final Research Achievements |
Rac1, which is one of the GTPases of the Rho subfamily, has crucial role for cytoskeletal architecture and the regulation of cell migration and growth. However, renal injury in mice with podocyte-specific deletion of Rac1 has yet to be elucidated fully due to conflicting findings. Here, we identified the possible role for Rac1 in podocytes of streptozotocin (STZ) induced diabetic mice. Our results provided the evidence that podocyte-specific deletion of Rac1 results in morphological alteration in podocyte, and induction of apoptosis or decreased expression of the slit diaphragm proteins by hyperglycemic stimuli are associated with progression of diabetic nephropathy.
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Report
(4 results)
Research Products
(4 results)
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[Journal Article] Podocyte-specific deletion of Rac1 leads to aggravation of renal injury in STZ-induced diabetic mice2015
Author(s)
Masanori Ishizaka, Tomohito Gohda, Miyuki Takagi, Keisuke Omote, Yuji Sonoda, Juan Alejandro Oliva Trejo, Rin Asao, Teruo Hidaka, Katsuhiko Asanuma, Satoshi Horikoshi, Yasuhiko Tomino
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Journal Title
Biochemical and Biophysical Research Communications
Volume: 467
Issue: 3
Pages: 549-555
DOI
Related Report
Peer Reviewed / Int'l Joint Research / Acknowledgement Compliant
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