2013 Fiscal Year Final Research Report
Dysfunction of multipotent pericytes as the primary cause of overactive bladder
Project/Area Number |
23659763
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Research Category |
Grant-in-Aid for Challenging Exploratory Research
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Allocation Type | Multi-year Fund |
Research Field |
Urology
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Research Institution | Nagoya City University |
Principal Investigator |
HASHITANI HIKARU 名古屋市立大学, 医学(系)研究科(研究院), 教授 (10315905)
|
Co-Investigator(Kenkyū-buntansha) |
TAKANO Hiromichi 名古屋市立大学, 大学院医学研究科, 助教 (70410313)
MITSUI Retsu 名古屋市立大学, 大学院医学研究科, 助教 (90434092)
|
Project Period (FY) |
2011 – 2012
|
Keywords | ペリサイト / 微小循環 / 自動運動 / 組織酸性化 / 過活動膀胱 |
Research Abstract |
Mural cells in bladder suburothelial venules exhibit spontaneous Ca2+ transients arising from IP3-mediated Ca2+ release from sarcoendoplasmic reticulum. Electrical coupling depending on the regenerative nature of L-type Ca2+ channels play a critical role in maintaining intercellular synchrony amongst mural cells. Spontaneous venular constrictions contribute to active drainage of tissue metabolites, and appear to be regulated by sympathetic innervations as well as bioactive substances released from urothelium and detrusor smooth muscle. Mural cells in suburothelial microvasculature consist of NG2(-)/alphaSMA(+) venular mural cells, NG2(+)/alphaSMA(-) capillary pericytes and NG2(+)/alphaSMA(+) arteriolar smooth muscle cells, suggesting that the origin or process of differentiation of venular mural cells may be distinct from that of mural cells in capillary or arteriole.
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Research Products
(21 results)