Antibody-array technique reveals overexpression of important DNA-repair proteins during cardiac ischemic preconditioning.
It is well known that repetitive ischemia followed by reperfusion (four cycles of 5 min of ischemia and 10 min of reperfusion) demonstrates protective effect against subsequent severe ischemic insult, known as ischemic preconditioning (PC). This phenomenon causes reduction in oxidative DNA damage, infarct size, and the extent of apoptotic cell death, leading to adaptation on functional recovery. The involvement of DNA-repair mechanisms in PC has not been well studied. We utilized the antibody-array technique to identify DNA-repair proteins that were upregulated by ischemic PC in the permanent left anterior coronary artery occlusion myocardial infarction (MI) model. The antibody-array system enabled us to identify three double-strand-break-repair proteins--Rad50, DNA topoisomerase I, Ku80--that were upregulated and might be involved in cell-survival processes during adaptation. With Western blot analysis, we found no significant difference in Ku80 protein expression between preconditioned and control groups after MI. Therefore, this report focuses on the overexpression of Rad50 and DNA topoisomerase and proposes that the DNA-repair mechanism in the permanent left anterior descending coronary artery (LAD) occlusion model involves these two proteins.[1]References
- Antibody-array technique reveals overexpression of important DNA-repair proteins during cardiac ischemic preconditioning. Mathur, P., Kaga, S., Zhan, L., Das, D.K., Maulik, N. J. Mol. Cell. Cardiol. (2005) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
