| Project/Area Number |
05454274
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Kyushu University |
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Principal Investigator |
SHIMOKAWA Hiroaki Kyushu University Assoc.Prof., 医学部, 助教授 (00235681)
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| Co-Investigator(Kenkyū-buntansha) |
UENO Hikaru Kyushu University Assis.Prof., 医学部, 講師 (50260378)
SUEISHI Katsuo Kyushu University Professor, 医学部, 教授 (70108710)
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| Project Period (FY) |
1993 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥6,600,000 (Direct Cost: ¥6,600,000)
Fiscal Year 1994: ¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 1993: ¥3,700,000 (Direct Cost: ¥3,700,000)
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| Keywords | inflammatory cytokines / ischemic heart disease / arteriosclerosis / coronary artery spasm / coronary thrombosis / myocardial infarction / サイトカイン / 細胞増殖因子 / 冠動脈硬化 / 冠等縮 / 冠□縮 |
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| Research Abstract |
(A)Basic Research
(1) Chrocic Treatment with interleukin (IL) -1beta causes arteriosclerotic changes and vasospastic responses to autacoids in porcine coronary arteries in vivo.
(2) Chronic treatment with IL-1alpha or tumor necrosis factor-alpha (TNF-alpha) also caused similar changes of the coronary artery, showing the redundant effects of inflammatory cytokines.
(3) The histological and functiona changes of the coronary artery induced by IL-1beta were mediated by both platelet-derived growth factor and fibroblast growth factor-2.
(4) A selective tyrosine kinase inhibitor, ST638, markedly suppressed the histological and functional changes of the coronary artery induced by IL-1beta.
(5) In the pathogenesis of coronary artery spasm at the inflammatory coronary lesions, a PKC-mediated pathway plays an important role, while the contribution of Ca^<2+>release from the intracellular store site may be minimal.
(B)Clinical Research
(6) Three types of changes in the plasma levels of cytokines were noted in patients with acute myocardial infarction ; transient increase (plasma levels of IL-6, generation capacity for IL-1alpha), sustained increase (plasma levels of macrophagecolony stimulating factor and generation capacity for IL-1beta), and late increase (plasma levels of interferon-gamma).
(7) In patients with ischemic heart disease, plasma levels of macrophage colony stimulating factor were increased, while those of transforming growth factor-beta were decreased.
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