| Project/Area Number |
24590371
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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 |
Pathological medical chemistry
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| Research Institution | Tohoku Medical and Pharmaceutical University (2016)
Tohoku University (2012-2015) |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
MORITO Naoki 筑波大学, 医学医療系, 講師 (70463825)
ABE Michiaki 東北大学, 大学病院, 講師 (40400246)
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| Project Period (FY) |
2012-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
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| Keywords | メサンギウム細胞 / 腎臓病 / 虚血再還流障害 / GATA因子 / 尿細管 / GATA3 / トランスジェニックマウス / 糸球体腎炎 / 炎症性サイトカイン / GATA転写因子 / 腎集合管細胞 / マクロファージ / GATA2 / 腎集合管 / アクアポリン / 虚血再還流 |
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| Outline of Final Research Achievements |
We demonstrated that zinc finger transcription factors,i.e., GATA2 and GATA3 is specifically expressed in renal collecting duct cells and glomerular mesangial cells, respectively. GATA3 plays a critical role for maintenance of the glomerular mesangial cells. Hence, GATA3-deficiency led to the occurence of spontaneous glomerulonephritis. GATA2 regulates a series of genes involved in water-reabsorption. Therefore, renal tubular cell-specific GATA2-deficient mice exhibited higher amount of urine. GATA2 also participates in the regulation of induced expression of inflammatory cytokine genes in the diseased kidney. The renal tubular cell-specific GATA2-deficient mice showed reduced expression level of the inflammatory cytokine genes and resistance against acute kidney injury. Furthermore, a newly identified GATA-inhibitor nicely ameliorated renal damages in the diseased kidney. Collectively, we propose that GATA2 can be a potential therapeutic target for the inflammatory kidney diseases.
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