| Project/Area Number |
10670644
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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 | Mie University |
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Principal Investigator |
IMAI Hiroshi (1999) Mie University, Faculty of Medicine, Research Associate, 医学部, 助手 (70300944)
吉田 恭子 (今中 恭子) (1998) 三重大学, 医学部, 助手 (00242967)
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| Co-Investigator(Kenkyū-buntansha) |
HARA Mari Mie University, Faculty of Medicine, Teaching Assistant, 医学部, 教務職員 (30176383)
SAKAKURA Teruyo Mie University, Faculty of Medicine, Professor, 医学部, 名誉教授 (80073120)
今井 裕 三重大学, 医学部, 助手 (70300944)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,800,000 (Direct Cost: ¥3,800,000)
Fiscal Year 1999: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1998: ¥2,700,000 (Direct Cost: ¥2,700,000)
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| Keywords | Extracellular matrix / tenascin / myofibroblast / knockout mouse / myocardial infarction / myocarditis / 筋繊維芽細胞 / 心疾患 |
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| Research Abstract |
In order to study the biological function, recombinant protein of tenascin-C was added to the cell cultures.
1) Tenascin-C, collaborating with fibronectin, accelerates the initial attachment of cardiomyocytes isolated from adult rat to laminin, however, tenascin-C is not involved in the formation of costameric attachment. 2) Tenascin-C induces the differentiation of fibroblasts to myofibroblasts. Secondary, to clarify the role of tenascin-C if myocardial tissue in vivo, we examined the wound healing of a mouse myocardial infarction model using tenascin-C knockout mouse. In tenascin-C null mutant, the number of smooth-muscle actin-positive cells was delayed to compare to that of normal mouse, however, healing proceeded normally. Tenascin-X, another member of tenascin family was ubiquitously expressed in normal heart, and slightly unregulated after myocardial injury at later stage. Our findings did not suggested that tenascin-X compensates for the loss of tenascin-C. Finally, to examine the possibility of the clinical application anti tenascin-C, we have established a new autoimmune mouse model. We also raised a mouse monoclonal antibody, which recognizes mouse tenascin-C by immunization of a tenascin-C knock out mouse. Immunoshitological study showed that tenascin-C expressed at very early stage of active phase of myocarditis. Our data demonstrate that tenascin-C is a useful marker for histological diagnosis to evaluate disease activity of myocarditis.
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