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Am J Physiol Heart Circ Physiol 287: H2468-H2477, 2004. First published July 29, 2004; doi:10.1152/ajpheart.01187.2003
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Overexpression of human heme oxygenase-1 attenuates endothelial cell sloughing in experimental diabetes

Nader G. Abraham,1,3 Rita Rezzani,4 Luigi Rodella,4 Adam Kruger,2 Derek Taller,1 Giovanni Li Volti,1 Alvin I. Goodman,2 and Attallah Kappas3

Departments of 1Pharmacology and 2Medicine, New York Medical College, Valhalla 10595; 3The Rockefeller University, New York, New York 10021; and 4Department of Biomedical Science, University of Brescia, Brescia, Italy 25124

Submitted 15 December 2003 ; accepted in final form 29 June 2004

Heme oxygenase (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, the number of circulating endothelial cells, and urinary 8-epi-isoprostane PGF2{alpha} (8-Epi) levels 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 and diminished in rats overexpressing HO-1. The number of detached endothelial cells and O2– formation increased in diabetic rats and in hyperglycemic animals underexpressing HO-1 and decreased in diabetic animals overexpressing HO-1 compared with controls. These data demonstrate that HO-1 gene transfer in hyperglycemic rats brings about a reduction in O2– 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.

gene transfer; circulating endothelial cells; superoxide; oxidative stress


Address for reprint requests and other correspondence: N. G. Abraham, New York Medical College, Valhalla, NY 10595 (E-mail: nader_abraham{at}nymc.edu)




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