| Project/Area Number |
23592376
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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 | Nagoya City University |
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Principal Investigator |
SASAKI Shoichi 名古屋市立大学, 医学(系)研究科(研究院), 准教授 (50225869)
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| Co-Investigator(Kenkyū-buntansha) |
KOJIMA Yoshiyuki 福島県立医科大学, 医学部, 教授 (60305539)
KUBOTA Yasue 名古屋市立大学, 大学院医学研究科, 講師 (00381830)
TAKADA Masa 名古屋市立大学, 大学院医学研究科, 研究員 (60468254)
KOHRI Kenjiro 名古屋市立大学, 大学院医学研究科, 教授 (30122047)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 前立腺肥大症 / KIT陽性間質細胞 / SCF / KIT陽性細胞 / KＩＴ陽性細胞 / 前立腺 / JAK-STATシグナル伝達 |
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| Research Abstract |
We investigated the role of the KIT-mediated mechanism in benign prostatic hyperplasia (BPH), and discuss the pathophysiology of BPH and a candidate target of BPH medical therapy.KIT was expressed in PrSC and human prostate, indicating that these samples are suitable for examining the function of KIT.Immunohistochemical analysis demonstrated that KIT was localized in interstitial cells (ICs) of the stromal component in human prostate. Administration of imatinib mesylate dose-dependently inhibited cell proliferation of PrSC with downregulation of JAK2 and STAT1, which are the main pathways downstream of SCF/KIT signal. SCF promoted cell proliferation of PrSC with upregulation of JAK2 and STAT1. KIT expression and the number of KIT-positive ICs in BPH were found to be significantly larger than in normal prostate.
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