Annual Research & Review in Biology

Abstract

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.