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1 Department of Pharmacology, New York Medical College, Valhalla, New York, USA; Laboratory of Pharmacology, The Rockefeller University, New York, New York, USA
2 Department of Biomedical Science, University of Brescia, Brescia, Italy
3 Department of Medicine, New York Medical College, Valhalla, New York, USA
4 Department of Pharmacology, New York Medical College, Valhalla, New York, USA
5 Laboratory of Pharmacology, The Rockefeller University, New York, New York, USA
* To whom correspondence should be addressed. E-mail: nader_abraham{at}nymc.edu.
Heme oxygenase-1 (HO-1) represents a key defense mechanism against oxidative injury. Hyperglycemia produces oxidative stress and various perturbations of cell physiology. The effect of streptozotocin (STZ)-induced diabetes on aortic HO activity, heme content, and the number of circulating endothelial cells and urinary 8-epi-isoprostane PGF2(8-EPI) in control rats and rats overexpressing or underexpressing HO-1 was measured. HO activity was decreased in hyperglycemic rats. Hyperglycemia increased urinary 8-EPI and this increase was augmented in rats underexpressing HO-1 key and diminished in rats overexpressing HO-1. The number of detached endothelial cells and superoxide formation increased in diabetic rats; and in hyperglycemic animals underexpressing HO-1 and decreased in diabetic animals overexpressing HO-1 compared to controls. These data demonstrate that HO-1 gene transfer in hyperglycemic rats brings about a reduction in superoxide production and a decrease in endothelial cell sloughing. Upregulation of HO-1 decreases oxidant production and endothelial cell damage and shedding and may attenuate vascular complications in diabetes.
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