2017 Fiscal Year Final Research Report
| Project/Area Number |
15K09241
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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 | University of Tsukuba |
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Principal Investigator |
Morito Naoki 筑波大学, 医学医療系, 講師 (70463825)
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| Research Collaborator |
USUI TOSHIAKI 筑波大学, 医学医療系, 講師
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Keywords | 糸球体上皮細胞 / 転写因子 |
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| Outline of Final Research Achievements |
Analysis of MafB deficient (MafB -/-) mice revealed that MafB is essential for podocyte differentiation and its foot process formation. However, the role of MafB in adult kidneys was not well known. Because MafB -/- mice die during the perinatal period, we used MafB heterozygote (MafB +/-) mice in this study.
We found that MafB +/- mice developed overt albuminuria at 50 week-old of age. By the electron microscopy analysis, we observed podocyte foot process effacement in MafB +/- mice. RT-PCR analysis revealed the Nephrin and Podocin glomerular expressions were decreased in MafB +/- mice compared to wild-type animals. We exploited transgenic mice expressing MafB in podocytes using Nephrin promoter (NPHS1 -MafB TG mice). We found that the NPHS1 MafB transgene successfully restored MafB mice to normal albuminuria at 50 week-old of age.
Conclusions: MafB is essential for the maintenance of podocytes. MafB could be a therapeutic target in chronic kidney disease.
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| Free Research Field |
腎臓内科学
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