Journal
CELL DEATH & DISEASE
Volume 4, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/cddis.2013.313
Keywords
ischemia; confocal; rat; oxymyoglobin
Categories
Funding
- OSU-HRS Fund [013000]
- OSU research resources from HRS and DHLRI
- OU General Fund [G110]
- Research Excellence Fund of Biomedical Research
- Shanghai Ruijin Hospital (China)
- UCSD research resources
Ask authors/readers for more resources
Myocardial ischemia-reperfusion (I/R) causes severe cardiac damage. Although the primary function of oxymyoglobin (Mb) has been considered to be cellular O-2 storage and supply, previous research has suggested that Mb is a potentially protective element against I/R injury. However, the mechanism of its protective action is still largely unknown. With a real-time fluorescent technique, we observed that at the onset of ischemia, there was a small burst of superoxide (O-2(center dot-)) release, as visualized in an isolated rat heart. Thus, we hypothesize that the formation of O-2(center dot-) correlates to Mb due to a decrease in oxygen tension in the myocardium. Measurement of O-2(center dot-) production in a Langendorff apparatus was performed using surface fluorometry. An increase in fluorescence was observed during the onset of ischemia in hearts perfused with a solution of hydroethidine, a fluorescent dye sensitive to intracellular O-2(center dot-). The increase of fluorescence in the ischemic heart was abolished by a superoxide dismutase mimic, carbon monoxide, or by Mb-knockout gene technology. Furthermore, we identified that O-2(center dot-) was not generated from the intracellular endothelium but from the myocytes, which are a rich source of Mb. These results suggest that during the onset of ischemia, Mb is responsible for generating O-2(center dot-). This novel mechanism may shed light on the protective role of Mb in I/R injury.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available