2020 Fiscal Year Final Research Report
Key oles of podocyte detyrosinated alpha-tubulin in the development of proteinuria
| Project/Area Number |
19K17744
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 53040:Nephrology-related
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| Research Institution | Okayama University |
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Principal Investigator |
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| Project Period (FY) |
2019-04-01 – 2021-03-31
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| Keywords | 蛋白尿 / ポドサイト / 微小管 / 翻訳後修飾 |
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| Outline of Final Research Achievements |
In this study, we examined the changes in detyrosination of α-tubulin in the kidney from proteinuric disease models. Detyrosinated α-tubulin was mainly expressed in podocytes in the kidney, and its expression was significantly reduced with podocyte injury in adriamycin nephropathy and high-fat diet proteinuric mice models. In addition, in vitro experiments showed that the expression of detyrosinated α-tubulin was regulated by PTEN/AKT/GSK-3β pathway in cultured immortalized podocytes. Taken together, this study suggests the involvement of α-tubulin detyrosination in proteinuric kidney diseases with podocyte injury.
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| Free Research Field |
腎臓内科学
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| Academic Significance and Societal Importance of the Research Achievements |
本研究は、腎臓における役割が不明であった微小管脱チロシン化αチューブリンが主として糸球体ポドサイトに発現しており、その発現は蛋白尿を発生する腎疾患において減少し、ポドサイト細胞内でPTEN/AKT/GSK3βシグナル経路による制御を受けていることを示したものであり、現在、直接的にポドサイトを標的とした腎疾患の治療法がない中で、蛋白尿を伴う腎疾患の機序の一部を解明し、微小管αチューブリンの脱チロシン化が新たな治療標的となる可能性を示した。
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