| Project/Area Number |
18K15126
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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 49030:Experimental pathology-related
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| Research Institution | Fukushima Medical University |
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Principal Investigator |
Higashi Atsuko 福島県立医科大学, 医学部, 助教 (50557569)
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| Project Period (FY) |
2018-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2019: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2018: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | ネフローゼ症候群 / クローディン / ポドサイト / 密着結合 / claudin / スリット膜 / タイト結合 |
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| Outline of Final Research Achievements |
We investigated molecular components of newly formed tight junctions between widened foot processes of injured podocytes utilizing RNA-seq analysis of isolated glomeruli and producing highly specific monoclonal antibodies against each claudins, which are indispensable components of tight junction structure. Surprisingly, none of tight junction related proteins showed significant expression difference between healthy and injured glomeruli in RNA-seq. These result suggests that tight junction components are kept prevented to form junction structure in healthy podocyte under unknown mechanism.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究は、ネフローゼ症候群のポドサイトのスリット膜がタイト結合(密着結合）に置き換わる現象に着目し、スリット膜構造の維持に関わるメカニズムを明らかにするものである。将来的には、障害ポドサイトに出現するタイト結合が、細胞障害に対して防御的に働くかどうかを検証することに繋がり、ネフローゼ症候群の病態メカニズムに新しい視点からアプローチできることが期待される。
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