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Journal of Pharmacology And Experimental Therapeutics Fast Forward
First published on May 8, 2007; DOI: 10.1124/jpet.107.119479


0022-3565/07/3222-514-520$20.00
JPET 322:514-520, 2007
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CARDIOVASCULAR

Long-Term Treatment with the Apolipoprotein A1 Mimetic Peptide Increases Antioxidants and Vascular Repair in Type I Diabetic Rats

Stephen J. Peterson, Daniel Husney, Adam L. Kruger, Rafal Olszanecki, Francesca Ricci, Luigi F. Rodella, Alessandra Stacchiotti, Rita Rezzani, John A. McClung, Wilbert S. Aronow, Susumu Ikehara, and Nader G. Abraham

Departments of Medicine (S.J.P.), Cardiology (A.L.K., J.A.M., W.S.A.), and Pharmacology (D.H., R.O., N.G.A.), New York Medical College, Valhalla, New York; Department of Biomedical Science, University of Brescia, Italy (F.R., L.F.R., A.S., R.R.); and Kansai Medical University, Osaka, Japan (S.I.)

Apolipoprotein A1 mimetic peptide (D-4F), synthesized from D-amino acid, enhances the ability of high-density lipoprotein to protect low-density lipoprotein (LDL) against oxidation in atherosclerotic disease. Using a rat model of type I diabetes, we investigated whether chronic use of D-4F would lead to up-regulation of heme oxygenase (HO)-1, endothelial cell marker (CD31+), and thrombomodulin (TM) expression and increase the number of endothelial progenitor cells (EPCs). Sprague-Dawley rats were rendered diabetic with streptozotocin (STZ) and either D-4F or vehicle was administered, by i.p. injection, daily for 6 weeks (100 µg/100 g b.wt.). HO activity was measured in liver, kidney, heart, and aorta. After 6 weeks of D-4F treatment, HO activity significantly increased in the heart and aorta by 29 and 31% (p < 0.05 and p < 0.49), respectively. Long-term D-4F treatment also caused a significant increase in TM and CD31+ expression. D-4F administration increased antioxidant capacity, as reflected by the decrease in oxidized protein and oxidized LDL, and enhanced EPC function and/or repair, as evidenced by the increase in EPC endothelial nitric-oxide synthase (eNOS) and prevention of vascular TM and CD31+ loss. In conclusion, HO-1 and eNOS are relevant targets for D-4F and may contribute to the D-4F-mediated increase in TM and CD31+, the antioxidant and anti-inflammatory properties, and confers robust vascular protection in this animal model of type 1 diabetes.


Received January 5, 2007; accepted May 2, 2007.

Address correspondence to: Dr. Nader G. Abraham, Department of Pharmacology, New York Medical College, Valhalla, NY 10595. E-mail: nader_abraham{at}nymc.edu




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