| Project/Area Number |
14370081
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Experimental pathology
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| Research Institution | Kyoto Prefectural University of Medicine |
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Principal Investigator |
TAKAMATSU Tetsuro Kyoto Prefectural University of Medicine, School of Medicine, Professor, 医学研究科, 教授 (40154900)
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| Co-Investigator(Kenkyū-buntansha) |
TANAKA Hideo Kyoto Prefectural University of Medicine, School of Medicine, assistant professor, 医学研究科, 助手 (60236619)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥11,300,000 (Direct Cost: ¥11,300,000)
Fiscal Year 2003: ¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 2002: ¥7,600,000 (Direct Cost: ¥7,600,000)
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| Keywords | Myocardial infarction / Calcium ion / Gap junction / Arrhythmia / Real-time confocal microscope |
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| Research Abstract |
To know how abnormal intracellular Ca^<2+> dynamics and gap junctional communication are integrated into arrhythmia, we visualized the intracellular Ca^<2+> dynamics by in situ Ca^<2+> imaging and expression of connexin 43 by GFP technique in ischemic rat hearts. Based on the hypothesis that Ca^<2+> waves would arise at the border zone of the infarction as a consequence of Ca^<2+> overload, we conducted in situ Ca^<2+> imaging. The subepicardial myocytes at the border zone showed abnormal intracellular calcium handling and gap junctional intercellular communication, such as stimulation-induced Ca^<2+> waves, which were evoked exclusively on electrical stimulation, instead of Ca^<2+> transients. These abnormal [Ca^<2+>]_i dynamics are supposed to be an important substrate for arrhythmias in ischemic hearts. We also made an EBV-based plasmid encoding connexin43-mRFP fusion protein for elucidating effects of abnormal gap junctional communication on ventricular conductivity. The EBV-based plasmid has different fluorescent wavelength spectrum from that of a calcium indicator, fluo-3,and were infused into the aortic root of rats. To maximize delivery, the aortic root was transiently occluded during a brief asystole. We concluded that these techniques could substantially contribute to our understanding of relationship between intracellular Ca^<2+> dynamics and expression of connexin 43 in ischemic rat hearts.
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