| Project/Area Number |
24592450
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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 |
Urology
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| Research Institution | Nara Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
HIGASHIHARA Eiji 杏林大学, 医学部, 教授 (00092312)
NAGAO Shizuko 藤田保健衛生大学, 医学部・疾患モデル教育研究センター, 准教授 (20183527)
CHIHARA Yoshitomo 奈良県立医科大学, 医学部, 講師 (40405395)
KOJIMA Naoto 京都薬科大学, 薬学部, 講師 (90420413)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥520,000 (Direct Cost: ¥400,000、Indirect Cost: ¥120,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2012: ¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
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| Keywords | 多発性嚢胞腎 / ＰＣＫラット / 細胞マトリックス / ベンゾイソフラノン誘導体 / ラットＰＣＫ / 細胞外マトリクス / ＤＮＡメチル化 / ベンゾイソフラノン化合物 |
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| Outline of Final Research Achievements |
We studied the mechanism of progression of polycystic kidney disease explored by the pathological pictures of PCK rat kidneys of 5-week old male, treated with Benzoisofuranone derivatives for five weeks, and the epigenetic modification of cellular matrix-adhesion protein genes such as HIF-1, Galectin-3, DNMT1, Mlana, RTL1, Gypsy integrase-1 (Gin1) in frozen PCK kidney tissues. The pathology of beneficial findings of PCK rat kidney treated, showed stabilization of ductal tubules and that of peri-ductal capillary without sludging of blood, and minimization of cystic mass growing. The response of HIF-1 mRNA expression of frozen kidney was decreased with concomitant increase of DNA methylation level, which is benefical response of anti-fibrosis of PCK kidney. An increase of mRNA expression of Mlana, having function of angiogenesis, and a decrease of that of Gin1 were observed. Those findings suggested that an epigenetic modification played a role in the progression of PCK kidneys.
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