Analysis Tools
growth/size/body
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• mice show a slight but significant decrease in body weight at 10 weeks of age but not at later times of development relative to wild-type controls
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cardiovascular system
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• at 10 weeks post-TAC, mice fail to show a strong induction of the pro-apoptotic protein Bax in the heart, unlike TAC-operated wild-type controls
• however, anti-apoptotic proteins Bcl2 and BclXL remain largely unchanged
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• after 10 weeks of trans-aortic constriction (TAC), mice show no signs of cardiac hypertrophy, no significant enlargement of the ventricular chambers, no deterioration of hemodynamic function, and no significant increase in cell surface area, unlike TAC-operated wild-type controls
• at 10 weeks, TAC-induced increases in heart weight/body weight ratio, cardiac fibrosis, re-expression of fetal cardiac genes, and induction of apoptosis are significantly attenuated relative to TAC-operated wild-type controls
• protection against pathological cardiac stress correlates with limited genetic fetal reprogramming, increased insulin receptor beta phosphorylation, as well as PKA and ephrin receptor expression, and inactivation of deleterious pathways such as CaMKIIdelta/PLC signaling
• however, mice do not develop any spontaneous pathology and have a normal cardiac phenotype under basal conditions
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homeostasis/metabolism
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• after 10 weeks of trans-aortic constriction (TAC), mice show no signs of cardiac hypertrophy, no significant enlargement of the ventricular chambers, no deterioration of hemodynamic function, and no significant increase in cell surface area, unlike TAC-operated wild-type controls
• at 10 weeks, TAC-induced increases in heart weight/body weight ratio, cardiac fibrosis, re-expression of fetal cardiac genes, and induction of apoptosis are significantly attenuated relative to TAC-operated wild-type controls
• protection against pathological cardiac stress correlates with limited genetic fetal reprogramming, increased insulin receptor beta phosphorylation, as well as PKA and ephrin receptor expression, and inactivation of deleterious pathways such as CaMKIIdelta/PLC signaling
• however, mice do not develop any spontaneous pathology and have a normal cardiac phenotype under basal conditions
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cellular
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• at 10 weeks post-TAC, mice fail to show a strong induction of the pro-apoptotic protein Bax in the heart, unlike TAC-operated wild-type controls
• however, anti-apoptotic proteins Bcl2 and BclXL remain largely unchanged
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muscle
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• at 10 weeks post-TAC, mice fail to show a strong induction of the pro-apoptotic protein Bax in the heart, unlike TAC-operated wild-type controls
• however, anti-apoptotic proteins Bcl2 and BclXL remain largely unchanged
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