1995 Fiscal Year Final Research Report Summary
A study on the mechanism of transformation of the hypertrophied myocardium in infants, children and adults
| Project/Area Number |
06670746
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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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 | Tokyo Women's Medical College |
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Principal Investigator |
NISHIKAWA Toshio Tokyo Women's Medical College, Associate Professor, 医学部, 助教授 (50120019)
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| Co-Investigator(Kenkyū-buntansha) |
ISHIHARA Kazuaki Iwate Medical College, Assistant Professor, 医学部, 講師 (30119888)
ANDO Akiko Tokyo Women's Medical College, Assistant, 医学部, 助手 (90232090)
MASUDA Masahiro Tokyo Women's Medical College, Assistant Professor, 医学部, 講師 (60209434)
KASAJIMA Takeshi Tokyo Women's Medical College, Professor, 医学部, 教授 (30045653)
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| Project Period (FY) |
1994 – 1995
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| Keywords | Hypertrophied myocardium / Transformation / Cytoskelton / Interstitial cell / Immunohistochemistry / Molecular biology |
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| Research Abstract |
This study was designed to investigate the the morphological change and the desmin distribution in the hypertrophied myocytes and interstitial cells in the diseased heart of human and experimental rats by the methods of histopathology, immunohistochemistry and molecular biology. Light-microscopical examination revealed myocyte hypertrophy, disarrangement of muscle bundle and interstitial fibrosis in dilated cardiomyopathy of infants and children. Electronmicroscopy revealed scarcity of myofibrils, mitochondriosis and proliferation of rough-surfaced endoplasmic reticulum and Golgi apparatus. The latter findings may suggest an increase in protein synthesis in the myocyte. Similar aspects except for scarcity of myofibrils were observed in the myocardium from patients with Tetralogy of Fallot. Desmin filaments were increased in number and characterized by a disordered arrangement in the hypertrophied myocytes in dilated cardiomyopathy. Desmin immunolabeling was transversely and longitudina
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ly distributed at the Z band level in the cytoplasm of these cells. Myocytes with disordered arrangement of desmin showed distinct expression of natriuretic peptides, while negative expression of them was revealed in the myocytes with normally arranged desmin. In situ hybridization showed increase in expression of desmin mRNA in the right ventricle of the pulmonary artery-binding rat heart, where mRNA of natriuretic peptides or alpha-skeletal muscle actin was also expressed. Interstitial fibroblastic cells proliferated in the myocardial tissue in dilated cardiomyopathy, dilated-phase hypertrophic cardiomyopathy, myocardial infarction and congenital heart disease with ventricular dilatation showed positive immunoreactivity for alpha-smooth muscle actin. They also revealed positive reactivity for embryonic isoform of non-muscle myosin heavy chain. These cells are suggested to be myofibroblasts by the ultrastructural aspects including filament insersion site, abundant actin filaments and discontinuous basement membranes. These results indicate that hypertrophied myocytes show various morphological changes with transformation and interstitial fibroblastic cells also transform in the myocardial tissue of the diseased heart in infants, children and adults. Less
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