2005 Fiscal Year Final Research Report Summary
Analysis of dynamics of splenic sinus endothelial cells for controlling of blood cell passage
| Project/Area Number |
16590159
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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 |
General anatomy (including Histology/Embryology)
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| Research Institution | Fukuoka University |
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Principal Investigator |
UEHARA Kiyoko Fukuoka University, School of Medicine, Associate Professor, 医学部, 助教授 (00084244)
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| Co-Investigator(Kenkyū-buntansha) |
KIYANAGI Midori Fukuoka University, School of Medicine, Assistant, 医学部, 助手 (20153687)
TANAKA Yoko Fukuoka University, School of Medicine, Assistant, 医学部, 助手 (10207152)
UEHARA Akira Fukuoka University, School of Medicine, Associate Professor, 医学部, 助教授 (60140745)
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| Project Period (FY) |
2004 – 2005
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| Keywords | sinus endothelial cells / store-operated Ca2+ influx / transient receptor potential channel / adherens junction / vascular endothelial cadherin / catenin / spleen / rat |
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| Research Abstract |
Endothelial cells of the splenic sinus have been previously investigated as a critical site for controlling blood cell passage through the splenic cord. For endothelial functionality, modulation of free cytosolic calcium ([Ca^<2+>]i) in response to humoral factors or hemodynamic forces is an essential step of intracellular transduction. Intracellular Ca^<2+> is a second messenger mediating a variety of important vascular endothelial cell functions, including the production of vasoactive substances, cell proliferation, gene expression, cytoskeleton remodelling, cell contraction, and disassembly of VE-cadherin with consequent increase in endothelial permeability. Mobilization of [Ca^<2+>]i is mediated by receptor-mediated Ca^<2+> channels, Ca^<2+> release from endoplasmic reticulum, store-operated calcium channels (SOCs) closely correlated with transient receptor potential (TRP) channels, and Ca^<2+> entry through mechanosensitivity, among others. Inosito-1,4,5-trisphosphate receptors (I
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P_3R) and RyR are the main conduit for the regulated release of Ca^<2+> from intracellular stores, and coupling of IP_3R and RyR to TRP channels has been reported. In addition to inosito-1,4,5-trisphosphate mediated Ca^<2+> mobilization and Ca^<2+> release from ryanodine-sensitive pools, Ca^<2+>-influx through TRP channels has also been suggested to be an important component in endothelial Ca^<2+>-signaling.
In the present study, the presence and ultrastructural localization of TRPC1 and the closely associated channels and proteins, IP_3R,RyR,VE-cadherin, and CRT, in the sinus endothelial cells of rat spleen were examined by confocal laser scanning microscopy and transmission electron microscopy to elucidate the role of TRPC1 in signal transduction in sinus endothelial cells. Moreover, the localization of VE-cadherin, β-catenin, and p120-catenin in the rat spleen sinus endothelial cells was examined to characterize the presence and distribution of adherens junction formation mediated by the cadherin-catenin complex and immunolabeling was evident at various levels in the lateral junctional membranes and was intermittently observed in the sinus endothelium. Less
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