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2015 Fiscal Year Final Research Report

A Kit Ligand, Stem Cell Factor as a Possible Mediator Inducing Overactive Bladder

Research Project

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Project/Area Number 25462521
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Urology
Research InstitutionNagoya City University

Principal Investigator

Kubota Yasue  名古屋市立大学, 医学(系)研究科(研究院), 講師 (00381830)

Co-Investigator(Kenkyū-buntansha) SASAKI Shoichi  名古屋市立大学, 大学院医学研究科, 准教授 (50225869)
HAMAKAWA Takashi  名古屋市立大学, 大学院医学研究科, 助教 (40595394)
SIBATA Yasuhiro  名古屋市立大学, 大学院医学研究科, 助教 (10534745)
IMURA Makoto  名古屋市立大学, 大学院医学研究科, 研究員 (00551269)
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, 学長 (30122047)
Project Period (FY) 2013-04-01 – 2016-03-31
Keywords過活動膀胱 / Kit / 幹細胞因子 / バイオマーカー
Outline of Final Research Achievements

In the gastrointestinal tract, interstitial cells of Cajal (ICCs) act as primary pacemaker cells to generate slow wave activity, and play a fundamental role in the transmission of signals from enteric neurons to smooth muscle cells. ICCs have been also identified in the urinary bladder. KIT is used as an identification marker of ICCs, and KIT-positive ICCs are located throughout the bladder wall.
They may be involved in signal transmission between smooth muscle bundles, from efferent nerves to smooth muscles, and from urothelium to afferent nerves. Not only disturbance of spontaneous contractility caused by the altered dertusor ICC signal transduction between nerves and smooth muscle cells but also disturbance of signal transduction between urothelial cells and sensory nerves via suburethelial ICC may induce overactive bladder (OAB).
The blockage of c-kit receptor may offer a new therapeutic strategy for OAB treatment, although further study will be needed.

Free Research Field

排尿障害

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Published: 2017-05-10  

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