Project/Area Number |
15590305
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Human pathology
|
Research Institution | University of Miyazaki (2004) 宮崎医科大学 (2003) |
Principal Investigator |
HATAKEYAMA Kinta Miyazaki Univ., Pathology, Assistant, 医学部, 助手 (60325735)
|
Co-Investigator(Kenkyū-buntansha) |
ASADA Yujiro Miyazaki Univ., Pathology, Prof., 医学部, 教授 (70202588)
MARUTSUKA Kousuke Miyazaki Univ., Pathology, Assist Prof., 医学部, 助教授 (00239154)
YAMASHITA Atsushi Miyazaki Univ., Pathology, Assistant, 医学部, 助手 (90372797)
IMAMURA Takuroh Miyazaki Univ., Internal Medicine, Assist Prof., 医学部, 講師 (60203329)
佐藤 勇一郎 宮崎大学, 医学部, 助手 (90347055)
|
Project Period (FY) |
2003 – 2004
|
Project Status |
Completed (Fiscal Year 2004)
|
Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2004: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 2003: ¥1,900,000 (Direct Cost: ¥1,900,000)
|
Keywords | CD39 / ecto-ATPDase / Atherosclerosis / Acute coronary syndromes / Directional atherectomy / Plaque instability / Immunohistochemistry / Adenovirus vector / Gene transfer / 剖検症例冠動脈 |
Research Abstract |
Ecto-ATP diphosphohydrolase/CD39(CD39) regulates hemostasis, thrombogenesis and inflammatory response by hydrolyzing extracellular ATP and ADP. Expression of CD39 has been reported in the endothelial cells and medial smooth muscle cells in the vascular system, however, CD39 expression in the atherosclerotic lesions has not been addressed. To determine whether the expression of CD39 in coronary atherosclerotic lesions is related to plaque instability and thrombus formation, we immunohistochemically assessed specimens from patients with stable and unstable angina pectoris who had undergone directional coronary atherectomy(DCA). CD39 immunoreactivity was decreased in culprit lesions of unstable angina pectoris compared with those of stable angina pectoris, and reduced in DCA specimens with thrombus formation. These results suggest that CD39 expressed in atheromatous plaques plays an important role in preventing acute coronary syndromes. Furthermore, using rat carotid thrombosis model, we indicated that local expression of CD39 in injured arteries might prevent arterial thormbosis and subsequent neointimal growth.
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