2016 Fiscal Year Final Research Report
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 |
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| Section | 一般 |
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| Research Field |
Kidney internal medicine
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| Research Institution | Juntendo University |
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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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| Keywords | Rac1 / Diabetic nephropathy / Podocyte / Foot process effacement / Apoptosis |
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| 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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| Free Research Field |
腎臓内科学
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