2014 Fiscal Year Final Research Report
Clarification of pathophysiology of virus-associated acute encephalaopathy by evaluationg the function of tight junctions in vitro
| Project/Area Number |
24591581
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Pediatrics
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| Research Institution | Fukushima Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
KAWASAKI Yukihiko 福島県立医科大学, 医学部, 准教授 (00305369)
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| Co-Investigator(Renkei-kenkyūsha) |
HASHIMOTO Koichi 福島県立医科大学, 医学部, 准教授 (50322342)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Keywords | 脳症 / 血管内皮 / サイトカイン / タイトジャンクション |
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| Outline of Final Research Achievements |
The mechanism of endothelial injury caused by cytokines in severe virus-associated acute encephalopathy(AE) remains unclear. We established a method for estimating endothelial injury caused by TNFα, proinflammatory cytokine in vitro. Human umbilical vein endothelial cell (HUVEC) monolayers were treated with TNF-α, subsequently transendothelial electric resistance (TER) and permeability were measured using a impedance spectroscopy(cellZscope®), and FITC-conjugated dextran, respectively. Moreover, TNFα-induced morphological changes in claudin-5, one of the tight junction proteins, were observed by immunofluorescent staining. The decrease in TER, the time to TER recovery, and the increase in permeability were all dependent on TNF-α concentration. Delocalization of claudin-5 was also observed after TNF-α treatment. These methods are useful to clarify the mechanism of AE and subsequent vascular endothelial cells injury, and aid in the deve1opment of treatment options.
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| Free Research Field |
感染症
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