Fetal Myocardial Reduction in Hyperglycemic Mouse Pregnancy is Associated with Dys-regulated Expression of the Anti-apoptotic Gene Bcl-2 in the Developing Heart. Preliminary Results
J. Claudio Gutierrez, M. Renee Prater, Patricia Navarrete, Steven D. Holladay
Annual Research & Review in Biology · pp. 71–78 · Published 4 Oct 2013
10.9734/ARRB/2014/5085Abstract
Aims: We previously detected significant late-gestation ventricular myocardial reduction in fetal mouse hearts from hyperglycemic dams. Flow cytometric analysis of the myocardial cells showed an enhanced rate of apoptosis, suggesting dysregulated cell death as a mechanism associated with the myocardial defect. The present study therefore examined expression of the anti-apoptotic gene Bcl-2 in fetal myocardium from hyperglycemic mouse dams on days 14 and 17 of gestation. Methodology: The hyperglycemia was induced in female Rockefeller (inbred CD1) mice, 6 to 8 weeks old, by pre-breeding streptozotocin (STZ) injection. Results: Expression of Bcl-2 in the fetal myocardium from the diabetic dams was decreased by 53% and 51% at GD14 and 17, respectively. Conclusion: These results suggest maternal hyperglycemia may damage the developing myocardium by altering expression of gene pathways that regulate cell death.
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