All Phenotypes Nr3c1<tm1.1Jaci> MGI Mouse

premature death ( J:201995 )

• increase morbidity and mortality by 5 months

• 7 months median survival age

• male mice have a median survival age of 8 months while this is only 6 months for female mice

abnormal lung morphology ( J:201995 )

• free erythrocytes in alveoli and hemosiderin-laden macrophages (heart failure cells) within alveolar spaces (at 6 months of age

respiratory distress ( J:201995 )

enlarged heart ( J:201995 )

• in nearly all mice examined

increased heart weight ( J:201995 )

• at 3 months of age

cardiac hypertrophy ( J:201995 )

abnormal thoracic cavity morphology ( J:201995 )

• in the majority of mice examined

heart inflammation ( J:201995 )

• indicated by expression analysis

abnormal atrial thrombosis ( J:201995 )

• characterized by lamellation of fibrin and inflammatory cells, chronic inflammation, fibrosis, and neovascularization

abnormal calcium ion homeostasis ( J:201995 )

• isolated cardiomyocytes fail to show a sustained increase in intracellular calcium following exposure to low concentrations of caffeine

increased myocardial fiber size ( J:201995 )

• about a 140% increase in cardiomyocyte cross-sectional area at 3 months of age

• adrenalectomy at 2 months of age does not reduce the increase in cardiomyocyte size seen at 6 months of age

decreased heart left ventricle muscle contractility ( J:201995 )

• variable decrease in ejection fraction and increase in the left ventricular end-systolic dimension at 3 months of age

cardiovascular system phenotype ( J:201995 )

N	• despite cardiac remodeling and reduced heart function, no electrocardiogram abnormalities are detected in mice at 3 - 6 months of age

increased myocardial fiber size ( J:201995 )

• about a 140% increase in cardiomyocyte cross-sectional area at 3 months of age

• adrenalectomy at 2 months of age does not reduce the increase in cardiomyocyte size seen at 6 months of age

enlarged heart ( J:201995 )

• in nearly all mice examined

increased heart weight ( J:201995 )

• at 3 months of age

cardiac hypertrophy ( J:201995 )

increased heart left ventricle weight ( J:201995 )

• at 3 months of age

dilated heart left ventricle ( J:201995 )

• marked

thick ventricular wall ( J:201995 )

• at 3 months

cardiac fibrosis ( J:201995 )

• associated with atrial thrombosis

• NORMAL: not detected in the ventricular wall at 3 months of age

poor circulation ( J:201995 )

• atrial thrombosis is consistent with atrial blood stasis

decreased heart left ventricle muscle contractility ( J:201995 )

• variable decrease in ejection fraction and increase in the left ventricular end-systolic dimension at 3 months of age

abnormal heart echocardiography feature ( J:201995 )

• no abnormality in 1 month-old mice but byat 3 months, but not at 1 month, mutant mice displays spontaneous LV left ventricular systolic dysfunction.

abnormal myocardial fiber physiology ( J:201995 )

• isolated cardiomyocytes fail to show a sustained increase in intracellular calcium following exposure to low concentrations of caffeine

pathological neovascularization ( J:201995 )

• associated with atrial thrombosis

congestive heart failure ( J:201995 )

heart inflammation ( J:201995 )

• indicated by expression analysis

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

Contributing Projects: 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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