| Project/Area Number |
13670687
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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 |
Circulatory organs internal medicine
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| Research Institution | Tohoku University |
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Principal Investigator |
KAGAYA Yutaka Tohoku University Hospital ・ Lecturer, 医学部附属病院, 講師 (90250779)
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| Co-Investigator(Kenkyū-buntansha) |
GOTO Kaoru Yamagata University ・ School of Medicine ・ Professor, 医学部, 教授 (30234975)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥4,100,000 (Direct Cost: ¥4,100,000)
Fiscal Year 2002: ¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 2001: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | cardiac hypertrophy / heart failure / venticular remodeling / diacylglycerol / diacylglycerolkinase / single transduction / イノシトールリン脂質代謝 / アンジオテンシン変換酵素阻害薬 |
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| Research Abstract |
Diacylglycerol (DG) kinase (DGK) terminates signaling from DG, which serves as an activator of protein kinase C (PKC), by converting DG to phosphatidic acid. DGK is thus regarded as an attertuator of the PKC activity. In rats, five DGK isozymes have been cloned but little is known about their role in the heart. In this study the spatiotemporal expression of DGK isozymes was investigated in rat hearts under a normal condition and after myocardial infarction (MI) by in situ hybrization histochemistry and immunohistochemistry. In normal left ventricular (LV) myocardium, DGKα, -ε and -ζ mRNAs were expressed evenly throughout the myocardium, although the DGKα expression was very low. In infarcted hearts, the expression of DGKζ was enhanced in the peripheral zone of the necrotic area and at the border zone 3 and 7 days after MI, and to a lesser extent in the middle layer of the granulation tissue 21 days after MI. The enhanced DGKζ expression in the infarcted and border areas could be attributed to granulocytes and macrophages. In contrast, the expression of DGKε in the infarcted and border areas was lower than that in the viable LV throughout the postoperation period. Furthermore, DGKε expression in the viable myocardium 21 days after MI decreased significantly compared with LV myocardium in the sham-operated rats, and was completely restored by treatment with captopril. Our results demonstrate that three DGK isozymes are expressed in the heart and that each isozyme might have different functional characteristics in the healing and LV remodeling after MI.
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