Overexpression of human heme oxygenase-1 attenuates endothelial cell sloughing in experimental diabetes

被引：92

作者：

Abraham, NG ^{[1
]}

Rezzani, R

Rodella, L

Kruger, A

Taller, D

Volti, GL

Goodman, AI

Kappas, A

机构：

[1] New York Med Coll, Dept Pharmacol, Valhalla, NY 10595 USA

[2] New York Med Coll, Dept Med, Valhalla, NY 10595 USA

[3] Rockefeller Univ, New York, NY 10021 USA

[4] Univ Brescia, Dept Biomed Sci, I-25124 Brescia, Italy

来源：

AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY | 2004年 / 287卷 / 06期

关键词：

gene transfer; circulating endothelial cells; superoxide; oxidative stress;

D O I：

10.1152/ajpheart.01187.2003

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

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 PGF(2alpha) (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 O-2(-) 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 O-2(-) 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.

引用

页码：H2468 / H2477

页数：10

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