2012 Fiscal Year Final Research Report
Exploring the pathological mechanism of gap junction regarding the progression of athromatous plaque.
| Project/Area Number |
22591601
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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 |
Cerebral neurosurgery
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| Research Institution | 秋田県立脳血管研究センター (2012)
秋田県立脳血管研究センター(研究部門) (2010-2011) |
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Principal Investigator |
NAKASE Taizen 秋田県立脳血管研究センター, 脳卒中医療システム研究部, 部長 (60390928)
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| Project Period (FY) |
2010 – 2012
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| Keywords | 脳血管障害学 / 神経病理学 / 脳梗塞 / 動脈硬化 |
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| Research Abstract |
Fragility of atheromatous plaque in the internal cervical artery can be a risk of brain infarction. The activation of macrophage by oxidative stress, the vulnerability of vascular endothelial cell and the thrombogenesis of plaque have been reported to participate in the fragility of atheromatous plaque. Therefore, from the view point of prevention of brain infarction, we investigated the factor which may influence on the stabilization of atheromatous plaque. The expression of connexin (Cx) which composes gap junction, an intercellular communication organ, was immunohistochemicaly observed in the atheromatous plaques of human operation sample. As the results, Cx37 and Cx43 subtypes were related to the stabilization of the plaque affected by oxidative stress and the plaque independent from oxidative stress, respectively. It is suggested that each subtype of Cx may have different effect on the pathogenesis of atheromatous plaque.
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