mortality/aging
• mice do not survive past E14.5 with no live mice found in newborn litters
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cardiovascular system
• fine, abnormal trabecular structures
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• at E12.5, the thickness of the ventricular compact myocardial layer is reduced 61% compared to in wild-type mice
• at E14.5, the ventricular compact myocardial layer thickness is reduced 84% compared to in wild-type mice
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• conotruncal cushions are reduced in size and altered in location compared to in wild-type mice leading to abnormalities in ventriculoarterial positioning
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• endocardial cushions are hypoplastic at E12.5
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• mice exhibit a primum atrial septal defect unlike wild-type mice
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• mice exhibit a common atrioventricular canal and occasionally an unbalanced canal leading to a functionally univentricular heart
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• occasionally
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• mice exhibit large inlet-type ventricular septal defect
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• mice exhibit moderately hypoplastic and anteriorly malaligned left ventricular outflow tracts
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• the right ventricular outflow tract is more posteriorly positioned than in wild-type mice
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• mice exhibit a thinning of the ventricular wall
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hemorrhage
(
J:155855
)
• at E14.5, mice exhibit systemic hemorrhage
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• proliferation of cells in the ventricular myocardium is reduced by 51% at E12.5 and 55% at E14.5 compared to in wild-type mice
• however, apoptosis rates are normal
|
• at E14.5
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homeostasis/metabolism
muscle
• fine, abnormal trabecular structures
|
• at E12.5, the thickness of the ventricular compact myocardial layer is reduced 61% compared to in wild-type mice
• at E14.5, the ventricular compact myocardial layer thickness is reduced 84% compared to in wild-type mice
|
• proliferation of cells in the ventricular myocardium is reduced by 51% at E12.5 and 55% at E14.5 compared to in wild-type mice
• however, apoptosis rates are normal
|
cellular
• proliferation of cells in the ventricular myocardium is reduced by 51% at E12.5 and 55% at E14.5 compared to in wild-type mice
• however, apoptosis rates are normal
|