Increased DNA Damage and Decreased H-MYH Protein Expression in Human Myocardium with End-Stage Congestive Heart Failure
| Autor: | Chiming Wei, J. V. Conte, A. L. Lu-Chang, Y. Dong, R. Lin |
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| Rok vydání: | 2001 |
| Předmět: | |
| Zdroj: | Microscopy and Microanalysis. 7:72-73 |
| ISSN: | 1435-8115 1431-9276 |
| DOI: | 10.1017/s143192760002643x |
| Popis: | The reactive oxygen species (ROS) such as superoxide radical (O2), hydrogen peroxide (H2O2), and hydroxyl radical (OH), plays a critical role in the pathogenesis of hypertension, atherosclerosis, ischemia-reperfusion injury, stroke, myocardial infarction, and congestive heart failure. A recent study demonstrated that the frequency of mutation in a reporter gene increased in cortical DNA after forebrain ischemia-reperfusion. Eight DNA lesions that are characteristic of DNA damage mediated by free radicals were detected. Among the different oxidative-damage DNA products, 8-oXo-7,8-dihydrodeoxyguanine (8-oxoG) is the most stable and deleterious adduct. Recent studies demonstrated that human MutY homologue (hMYH) protein plays important role in repairing oxidative damage. to date, there is no information regarding the role of hMYH expression in human myocardium with congestive heart failure (CHF). Therefore, the current study designed to investigate the levels of hMYH expression and 8-oxoG in myocardium in the absence or presence of end-stage congestive heart failure. The hypothesis of this study is that increasing DNA damage such as 8-oxoG generation is associated with a reduction of hMYH expression in human myocardium with congestive heart failure. |
| Databáze: | OpenAIRE |
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