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 *
Department of Biomedical Sciences and Pathobiology, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Polytechnic Institute & State University, Blacksburg, VA, USA.
M. Renee Prater
Department of Biomedical Sciences, E. Via Virginia College of Osteopathic Medicine, Blacksburg, VA, USA.`
Patricia Navarrete
Pharmacology and Morphophysiology Institute, Austral University of Chile, Campus Isla Teja, Valdivia, Chile.
Steven D. Holladay
Department of Veterinary Biosciences and Diagnostic Imaging, University of Georgia, Athens, GA, USA.
*Author to whom correspondence should be addressed.
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.
Keywords: Diabetes mellitus, apoptosis, Bcl2, heart defects.