2010 Fiscal Year Final Research Report
Research for signal mechanism of the KIT-positive interstitial cells and development of the new molecular target treatment for the over active bladder
| Project/Area Number |
20591886
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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 | Nagoya City University |
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Principal Investigator |
SASAKI Shoichi Nagoya City University, 大学院・医学研究科, 准教授 (50225869)
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| Co-Investigator(Kenkyū-buntansha) |
KUBOTA Yasue 名古屋市立大学, 大学院・医学研究科, 講師 (00381830)
KOJIMA Yoshiyuki 名古屋市立大学, 大学院・医学研究科, 講師 (60305539)
OKADA Shinsuke 名古屋市立大学, 大学院・医学研究科, 研究員 (40381818)
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) |
2008 – 2010
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| Keywords | KIT陽性間質細胞 / 細胞増殖 / Glivec / Bcr-Abl / マウス / BOO(膀胱流出路閉塞)モデル / 過活動膀胱 / KIT変異ラット |
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| Research Abstract |
KIT is not only a detection marker of these cells, but also may play a crucial role in the control of bladder function. Research into the effect of c-kit receptor inhibitor, imatinib mesylate, on bladder function implies that KIT-positive ICCs may be therapeutic target cells to reduce bladder overactivity and that the blockage of c-kit receptor may offer a new therapeutic strategy for OAB treatment.
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Research Products
(35 results)
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[Journal Article] TRPM8-expressing dorsal root ganglion neurons project dichotomizing axons to both skin and bladder in rats.2011
Author(s)
Shibata Yasuhiro, Ugawa Shinya, Imura Makoto, Kubota Yasue, Ueda Takashi, Kojima Yoshiyuki, Ishida Yusuke, Sasaki Shoichi, Hayashi Yutaro, Kohri Kenjiro, Shimada Shoichi
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Journal Title
NeuroReport 185
Pages: 1053-1057
Peer Reviewed
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