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Role of ceramide in ischemic preconditioning
Jianhua Cui1, Richard M Engelman, Nilanjana Maulik
1Cardiovascular Research Center, School of Medicine, University of Connecticut Health Center, Farmington, CT 06030-1110, USA.
Journal of the American College of Surgeons
|April 28, 2004
Summary
Preconditioning increases heart ceramide and sphingosine-1-phosphate, offering protection against ischemia. This study suggests sphingolipids may induce Bcl-2 expression for pharmacological preconditioning (PC).
Area of Science:
- Cardiovascular Science
- Molecular Cardiology
- Biochemistry
Background:
- Myocardial preconditioning (PC) is associated with increased ceramide and sphingosine content.
- Sphingosine-1-phosphate, a ceramide metabolite, may act as an antiapoptotic factor.
- Hypothesis: Increased ceramide during PC is a protective mechanism.
Purpose of the Study:
- To investigate the role of sphingolipids in preconditioning-induced cardioprotection.
- To determine if desipramine affects PC-mediated changes in ceramide and sphingosine-1-phosphate.
- To assess the impact of desipramine on myocardial preservation during ischemia-reperfusion.
Main Methods:
- Isolated hearts subjected to ischemia-reperfusion.
- Groups included control, ischemia-reperfusion, desipramine treatment, PC, and PC with desipramine.
- Cardioprotection assessed via left ventricular function, infarct size, and cardiomyocyte apoptosis.
Main Results:
- PC improved ventricular recovery and reduced infarct size and apoptosis.
- Desipramine abolished PC's cardioprotective effects and downregulated Bcl-2.
- Desipramine blocked ceramide increase and inhibited sphingosine-1-phosphate increase during PC.
Conclusions:
- Sphingolipids may induce Bcl-2 expression, contributing to cardioprotection.
- Pharmacological preconditioning using sphingolipids warrants further investigation.
- Desipramine interferes with sphingolipid-mediated cardioprotective pathways.