Analysis Tools
normal phenotype
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• mice develop normally with normal life spans and cardiac structure and function and 18 week old hearts show no ventricular thinning, right ventricular dilatation or fibrosis
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Allele Symbol Allele Name Allele ID |
Tg(CMV-cat,-ROCK2*)3-1Koba transgene insertion 3-1, Kazuto Kobayashi MGI:5910536 |
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| Summary |
2 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice develop normally with normal life spans and cardiac structure and function and 18 week old hearts show no ventricular thinning, right ventricular dilatation or fibrosis
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 34.6% of mice die suddenly by 1 year of age
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• some sudden death of several pups before weaning at 4 weeks of age is seen
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• aortas are thinner
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• widening of the gaps at the intercalated discs in the myocardium of 25 week old mice
• desmosomes are less electron-dense than in controls at 25 weeks of age and the gap width at the desmosomes is increased
• distribution of desmosomal proteins is altered
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• right ventricle shows disorganized myocardial structure with poorly defined cell junctional areas
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• massive fat accumulation in the right ventricle free wall adjacent to areas of fibrosis is seen in 19 week old mice
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• heart weight to body weight ratio is increased
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• ventricular weight to body weight ratio is increased
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• thinning of interventricular septum of the hearts of E12.5 and E14.5 embryos
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• massive fat accumulation in the right ventricle free wall adjacent to areas of fibrosis is seen in 19 week old mice
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• thinning of ventricular walls of the hearts of E12.5 and E14.5 embryos
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• myocardial fibrotic changes are first evident at P3 in both the right and left ventricles
• fibrosis is initially seen in epicardial and perivascular regions of the ventricles, progressing to adjacent myocardium with age and involving the entire thickness of the right ventricle free wall at 19 weeks of age
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• hearts are markedly dilated as early as P3, with dilatation more prominent in the right ventricle and is progressive with age
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• progressive ventricular dilatation and thinning from P3
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• reduction in left ventricle ejection fraction and fractional shortening
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• reduction in the number of proliferating cardiomyocytes in the ventricular walls and interventricular septum (both in compact layer and trabeculated layer) in E12.5 hearts
• however, apoptosis levels are normal
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• echocardiography indicates dilated ventricular chambers, increased right ventricle and left ventricle dimensions, and reduced left ventricle ejection fraction and fractional shortening
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• mice frequently exhibit spontaneous ventricular arrhythmias, evident as long frequent runs of ventricular extrasystoles characterized by widened QRS complexes with no apparent association with the P waves
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• reduction in the number of proliferating cardiomyocytes in the ventricular walls and interventricular septum (both in compact layer and trabeculated layer) in adult hearts
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• systolic blood pressure is lower
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• mice develop arrhythmogenic right ventricular cardiomyopathy
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• reduction in the number of proliferating cardiomyocytes in the ventricular walls and interventricular septum (both in compact layer and trabeculated layer) in E12.5 hearts
• however, apoptosis levels are normal
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• widening of the gaps at the intercalated discs in the myocardium of 25 week old mice
• desmosomes are less electron-dense than in controls at 25 weeks of age and the gap width at the desmosomes is increased
• distribution of desmosomal proteins is altered
|
|
• right ventricle shows disorganized myocardial structure with poorly defined cell junctional areas
|
|
• massive fat accumulation in the right ventricle free wall adjacent to areas of fibrosis is seen in 19 week old mice
|
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• reduction in left ventricle ejection fraction and fractional shortening
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• reduction in the number of proliferating cardiomyocytes in the ventricular walls and interventricular septum (both in compact layer and trabeculated layer) in E12.5 hearts
• however, apoptosis levels are normal
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• mice develop arrhythmogenic right ventricular cardiomyopathy
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• heart weight to body weight ratio is increased
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| arrhythmogenic right ventricular cardiomyopathy | DOID:0050431 |
OMIM:PS107970 |
J:242116 | |
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO) |
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last database update 07/05/2024 MGI 6.24 |
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