| Project/Area Number |
15591697
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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 | Nagasaki University Graduate School of Biomedical Sciences |
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Principal Investigator |
NOGUCHI Mitsuru Nagasaki University Graduate School of Biomedical Sciences, Division of Nephro-Urology, Assistant, 大学院・医歯薬学総合研究科, 助手 (00325648)
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| Co-Investigator(Kenkyū-buntansha) |
KANETAKE Hiroshi Nagasaki University Graduate School of Biomedical Sciences, Division of Nephro-Urology, Professor, 大学院・医歯薬学総合研究科, 教授 (50100839)
NOMATA Koichiro Nomata Nagasaki University Hospital of Medicine and Dentistry, Division of Nephro-Urology, Lecturer, 医学部・歯学部附属病院, 講師 (80189430)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 2004: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 2003: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | Voiding dysfunction / Gap junction / Connexin 43 / Detrusor muscle / 排尿障害 |
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| Research Abstract |
Gap junctional intercellular communication may play an important role in cell growth, development and differentiation. Gap junctional intercellular channels allow direct movement between neighboring cells of ions, molecules and neurotransmitters less than 1.2 kDa. Therefore, it is considered that the gap junction may play an important role in synchronous detrusor contraction in voiding function. We investigated the alteration of gap junctional protein, connexin-43 (Cx-43) in rat detrusor muscle with voiding dysfunction model. Partial bladder outlet obstruction (BOO) rats and diabetes rats induced by streptozotosin were used for voiding disfunction model. Eight weeks later, cystmetrical investigation, alteration of the Cx-43 expression and extracellular signal-regulated kinase (ERK1/2) in detrusor muscle were analyzed. No detrusor contraction was observed in only BOO rat at 8 weeks. Cx-43 was expressed on cell membranes of detrusor muscle in control and DM rats. However, Cx-43 was revealed internal localization from cell membrane to cytoplasm or nuclei. The expression levels of phosphorylated Cx-43 of detrusor muscle in BOO were higher than those of control and DM rats. Furthermore, ERK1/2 activation of detrusor muscle in only BOO rats. Cx-43 of the detrusor mousle in BOO might be regulated by phosphorylation and ERK 1/2 activation, and the alterations of Cx-43 were considered to cause disruptions of gap junctions. These data suggest that the disruptions of gap junction in detrusor muscle may be one of the causes of voiding dysfunction.
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