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Phenotypes Associated with This Genotype
Genotype
MGI:5907611
Allelic
Composition
Tg(MT2A-TGFBR2)#Rser/0
Genetic
Background
involves: C57BL/6 * DBA
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No mouse lines available in IMSR.
See publication links below for author information.
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• under pressure-overload stress via transverse aortic constriction (TAC), mice receiving zinc in drinking water, show greatly reduced interstitial nonmyocyte proliferation in the left ventricle, attenuated collagen deposition in the left ventricle, increase in left ventricular end systolic diameter and end systolic and end diastolic volumes, decreased ejection fraction and fractional shortening

cardiovascular system
• at 28 and 120 days post-transverse aortic constriction (TAC), zinc-treated mice show no increase in collagen deposition in the left ventricle as is seen controls indicating attenuation of TAC-induced collagen deposition
• pressure-overload stress via TAC promotes left ventricular dilation in zinc-treated mice
• transverse aortic constriction of zinc-treated mice results in dilated cardiomyopathy, with mice showing exacerbated TAC-induced left ventricle dilation and dysfunction, but not left ventricle hypertrophy
• TAC-induced decrease in ejection fraction and fractional shortening are exacerbated in zinc-treated mice compared to controls
• however, cardiac output and heart rate are not different from controls following TAC
• at 120 days post-TAC, left ventricular end diastolic diameter and end diastolic volume are greater in zinc-treated mice than in controls
• TAC-induced increases in left ventricular end systolic diameter and end systolic volume are greater in zinc-treated mice than in controls at 120 days post-TAC
• under pressure-overload stress via transverse aortic constriction (TAC), mice receiving zinc in drinking water, show greatly reduced interstitial nonmyocyte proliferation in the left ventricle, attenuated collagen deposition in the left ventricle, increase in left ventricular end systolic diameter and end systolic and end diastolic volumes, decreased ejection fraction and fractional shortening

cellular
• TAC-induced nonmyocyte proliferation in left ventricle of zinc-treated mice is reduced 7 days post-TAC compared to controls
• however, apoptotic cell death in heart at 7 days after TAC is no different from controls

muscle
• transverse aortic constriction of zinc-treated mice results in dilated cardiomyopathy, with mice showing exacerbated TAC-induced left ventricle dilation and dysfunction, but not left ventricle hypertrophy
• TAC-induced decrease in ejection fraction and fractional shortening are exacerbated in zinc-treated mice compared to controls
• however, cardiac output and heart rate are not different from controls following TAC

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
dilated cardiomyopathy DOID:12930 OMIM:PS115200
J:158480


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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
10/29/2024
MGI 6.24
The Jackson Laboratory