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2015 Fiscal Year Final Research Report

Research on vesicular type transporter and refractory lower urinary tract dysfunction

Research Project

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Project/Area Number 26670699
Research Category

Grant-in-Aid for Challenging Exploratory Research

Allocation TypeMulti-year Fund
Research Field Urology
Research InstitutionUniversity of Yamanashi

Principal Investigator

TAKEDA Masayuki  山梨大学, 総合研究部, 教授 (80197318)

Co-Investigator(Renkei-kenkyūsha) ZAKOJI Hidenori  山梨大学, 総合研究部, 准教授 (60345717)
SAWADA Norifumi  山梨大学, 総合研究部, 助教 (70402055)
MIYAMOTO Tatsuya  山梨大学, 総合研究部, 助教 (80456459)
IHARA Tatsuya  山梨大学, 医学部附属病院, 診療助教 (90622407)
Project Period (FY) 2014-04-01 – 2016-03-31
Keywords下部尿路機能 / 難治性下部尿路機能障害 / 小胞型トランスポーター / 機械センサー / 時計遺伝子
Outline of Final Research Achievements

Micturition behabior was examined using a special metabolic cage. Male C57BL/6 mice aged 8-12 weeks old (WT) and male C57BL/6 ClockΔ19/Δ19 mice aged 8 weeks old were used. They were bred under 12-h light/dark conditions for 2 weeks and voiding behavior was investigated by measuring water intake volume, urine volume, urine volume/void, and voiding frequency in metabolic cages in the dark and light periods.ClockΔ19/Δ19 mice showed the phenotype of Nocturia(NC)/Nocternal Polyuria(NP). The ClockΔ19/Δ19 mouse may be used as an animal model of NOC and NP. We investigated the gene expression rhythms of the mechanosensory cation channels(TRPV4, Piezo1), and a main ATP release mediate molecules (ARMM)such as VNUT and Cx26 in the urothelium, in addition to clock genes.Disruption of circadian rhythms in mechano-sensors and ARMM, in addition to abnormalities in clock genes, could be one of the causes of NOC because of the hyper-sensitivity of bladder wall extension.

Free Research Field

泌尿器科学

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Published: 2017-05-10  

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