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1 Department of Pharmacology, New York Medical College, Valhalla, New York, USA
2 Department of Medicine, New York Medical College, Valhalla, New York, USA
3 Department of Physiology, New York Medical College, Valhalla, New York, USA
4 Department of Pathology, Kansai Medical University, Osaka, Japan
5 Department of Biomedical Sciences and Biotechnology, Division of Human Anatomy, University of Brescia, Brescia, Italy
* To whom correspondence should be addressed. E-mail: nader_abraham{at}nymc.edu.
Increased heme oxygenase (HO)-1 activity attenuates endothelial cell apoptosis and decreases superoxide anion (O2-) formation in experimental diabetes by unknown mechanisms. We examined the effect of HO-1 protein and HO activity on EC-SOD, catalase, O2-, iNOS and eNOS levels, and vascular responses to acetylcholine (Ach) in control and diabetic rats. Vascular EC-SOD and plasma catalase activities were significantly reduced in diabetic compared to nondiabetic rats (p<0.05). Upregulation of HO-1 expression by intermittent administration of CoPP, an inducer of HO-1 protein and activity, conferred a robust increase in EC-SOD, but there was no significant change in Cu/Zn-SOD. Administration of SnMP, an inhibitor of HO-1 activity, decreased EC-SOD protein. Increased HO-1 activity in diabetic rats was associated with a decrease in iNOS, but increases in eNOS and plasma catalase activity. On the other hand, aortic ring segments from diabetic rats exhibited significant reduction in vascular relaxation to Ach, which was reversed with CoPP treatment. These data demonstrate that an increase in HO-1 protein and activity, i.e., CO and bilirubin production, in diabetic rats brings about a robust increase in EC-SOD, catalase and eNOS with a concomitant increase in endothelial relaxation and a decrease in O2-. These observations in experimental diabetes suggest that the vascular cytoprotective mechanism of HO-1 against oxidative stress requires an increase in EC-SOD and catalase.
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