1993 Fiscal Year Final Research Report Summary
Molecular Biological Study of Cardiomyopathy in animals and in human
| Project/Area Number |
03454255
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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 | Osaka University |
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Principal Investigator |
AZUMA Junichi Osaka University, Department of Internal Medicine III, lecturer, 医学部, 講師 (30144463)
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| Co-Investigator(Kenkyū-buntansha) |
IHARA Yoshiji Osaka University Hospital, Staff, 医学部・附属病院, 医員
TAKIHARA Keiko Department of Internal Medicine III, assistant professor, 医学部, 助手 (70252640)
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| Project Period (FY) |
1991 – 1993
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| Keywords | Cardiomyopathy / Myopathic hamster / Oncogene / Familial hypertrophic cardiomyopathy / Myosin heavy chain gene / Genetic disease / Point mutation / Myocardial hypertrophy |
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| Research Abstract |
The expression of immediate early gene (c-fos mRNA) was transiently induced after norepinephirine (NE) treatment in hamster hearts in vivo as well as in cultured neonatal rat myocytes. The expression of c-fos mRNA in the heart was more augmented in cardiomyopathic hamster(Bio 14.6) than in control hamster (RB) after 1.5 mg/kg of NE injection. Treadmill running for 1 hr after NE(0.1mg/kg) injection induced the expression of c-fos mRNA in the Bio 14.6 heart but not in RB heart. The mRNA level of alpha_1 adrenergic receptor was not increased in Bio 14.6 heart compared to that of RB heart. The present results suggest that the post-receptor enhancement of signal transduction pathway after alpha_1 adrenergic receptor in cardiomyopathic hamster heart, and the profitable management for cardiomyopathic patients with alpha_1 blocking agents.
The cardiac beta-myosin heavy chain (beta-MHC) gene was analyzed in Japanese patients with familial hypertrophic cardiomyopathy(HCM). We found missence mutation (606Val -> Met) of beta-MHC, which has been reported in several Caucasian HCM families. Another kind of mutation, found in Japanese for the first time, was the deletion of three nucleotides of 10th codon in the exon 3, which results in the delection of an amino acid, glycine. Although the analysis of beta-MHC gene could lead to the predicition of prognosis of the patients with HCM, we don't have effective therapy regimen yet, which is eagerly hunting for.
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