| Project/Area Number |
22591786
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Urology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
HOMMA Yukio 東京大学, 医学部附属病院, 教授 (40165626)
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| Co-Investigator(Kenkyū-buntansha) |
NOMIYA Akira 東京大学, 医学部附属病院, 助教 (30372379)
NISHIMATSU Hiroaki 東京大学, 医学部附属病院, 准教授 (60251295)
FUJIMURA Tetsuya 東京大学, 医学部附属病院, 講師 (50376448)
KOUICHI Masunaga 東京都健康長寿医療センター, 病院, 医員 (10404352)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 排尿学 / 細胞・組織 / 間質性膀胱炎 / 尿中マーカー / 慢性炎症 / 膀胱機能 / 動物モデル |
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| Research Abstract |
This study was conducted to elucidate the pathogenesis of interstitial cystitis (IC), chronic inflammatory disease of the urinary bladder with unidentified cause. To achieve this purpose, we’ve focused on the transmitters expressed on urothelium or secreted into urine of human IC patients. Also, we’ve assessed bladder histology immuno-histochemically.Unfortunately, no significant correlation between urine markers and IC symptoms has been identified so far. However, histochemistry analysis indicated that immune cells expressing CD11b and VEGF-A significantly increased in ulcer type IC. In addition, in bladder tissue of IC with Sjogren’s syndrome showed significant appearance of both CD4 and CD8 positive immune cells, all of which indicating different pathogenesis in each type of IC.In animal model experiments, we tried to produce ketamine induced cystitis rat model, however, at the moment, IC symptoms of findings were not produced. Also we’ve produced rat IC model using acrolein,he bladder tissue of which was assessed for TRPM8 expression. The rats showed dynamic change in urinary frequency and voided volume, but no significant change in TRPM8 expression was observed.The pathogenesis and pathophysiology of IC are still undefined and need further investigations.
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