1995 Fiscal Year Final Research Report Summary
Molecular physiological study of contractile element of failing heart
| Project/Area Number |
06454285
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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 | University of Tokyo General |
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Principal Investigator |
MOMOURA Shin-ichi University of Tokyo, Faculty of Medicine, Assistant Professor, 医学部(病), 助手 (10190985)
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| Co-Investigator(Kenkyū-buntansha) |
AOYAGI Teruhiko University of Tokyo, Faculty of Medicine, Assistant Professor, 医学部(病), 助手 (10251240)
TAKAHASHI Toshiuyki University of Tokyo, Faculty of Medicine, Assistant Professor, 医学部(病), 助手 (40236302)
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| Project Period (FY) |
1994 – 1995
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| Keywords | in vitro motility asaay / laser optical trap / centrifuge microscope / cardiac myosin / regulatory protein |
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| Research Abstract |
1. We have shown that catlytic products of ATP,ADP and Pi, have an inhibitory action on actomyosin sliding in vitro, This result suggests that cardac myosin is more resistant to ischemia than skeletal one. I intact muscle, ATP regenerating system provides optimal condition for ATP hydrolysis by myosin.
2. In vitro sliding of thin filament reconstituted from actin and troponin-tropomyosin complex was regulated by calcium concentration. Calcium sensitivity was reduced under various conditions such as acidosis and hypothermia, but reversed by calcium sensitizer. This effect of calcium sensitizer seemed to be mediated by regulatory protein.
3. We compared the force generating ability of cardiac myosin isoforms (V1 and V3) using two different in vitro force measuring systems, centrifuge microscope and laser optical trap. The two isoforms had different kinetic properties, but had similar force generating ability.
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