Analysis Tools
cardiovascular system
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• mutant hearts fail to thicken the ventricular wall after E14.5
• abnormalities in cardiomyocyte differentiation and cytoskeletal formation are likely to result from defects in TGF-beta/Smad signaling
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• at E11.5, 3 of 11 mutant hearts exhibit thickened myocardial fibers
• at E16.5, the distribution of dystrophin is disrupted and myofibril formation is absent from mutant hearts
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• at E15.5, no blood vessels are evident and mutant hearts are paler than wild-type hearts
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• at E14.5, 6 of 19 mutant hearts exhibit a ventricular septal defect
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small heart
(
J:219548
)
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• at E15.5, mutant hearts are smaller than wild-type
• however, no difference in heart size or appearance is observed through E12.5
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• at E14.5, the density of cells in the trabecular layer of mutant hearts is lower than that in wild-type hearts
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• at E14.5, the thicknesses of the compact layer of the left ventricle (LV) is significantly reduced, relative to that in wild-type embryos
• in contrast, the thickness of the LV trabecular layer is not significantly altered
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• the ventricle wall of mutant hearts fails to thicken after E14.5, unlike in wild-type hearts
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hemorrhage
(
J:200082
)
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• in 5 of 8 mice at E14.5
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• at E16.5, quantification of TUNEL-positive cells revealed that mutant ventricular cardiomyocytess show a 16-fold increase in apoptotic signal relative to controls
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• at E16.5, the proliferation of mutant ventricular cardiomyocytes is significantly reduced, as shown by phospho-histone H3 expression analysis and Ki-67 staining
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homeostasis/metabolism
muscle
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• at E14.5, the density of cells in the trabecular layer of mutant hearts is lower than that in wild-type hearts
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• at E14.5, the thicknesses of the compact layer of the left ventricle (LV) is significantly reduced, relative to that in wild-type embryos
• in contrast, the thickness of the LV trabecular layer is not significantly altered
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• at E16.5, quantification of TUNEL-positive cells revealed that mutant ventricular cardiomyocytess show a 16-fold increase in apoptotic signal relative to controls
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• at E16.5, the proliferation of mutant ventricular cardiomyocytes is significantly reduced, as shown by phospho-histone H3 expression analysis and Ki-67 staining
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cellular
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• at E16.5, quantification of TUNEL-positive cells revealed that mutant ventricular cardiomyocytess show a 16-fold increase in apoptotic signal relative to controls
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• at E16.5, the proliferation of mutant ventricular cardiomyocytes is significantly reduced, as shown by phospho-histone H3 expression analysis and Ki-67 staining
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• quantification of phospho-histone H3-positive cells revealed that the G2/M transiting signal is only 5% that of controls
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