© 2000 by European Society of Cardiology
Copyright © 2000, European Society of Cardiology
Ecto-5'-nucleotidase plays a role in the cardioprotective effects of heat shock protein 72 in ischemia–reperfusion injury in rat hearts
aDepartment of Surgery, Course of Interventional Medicine (E1), Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka 565-0871, Japan
bDepartment of Internal Medicine and Therapeutics, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka 565-0871, Japan
cDivision of Gene Therapy Science, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka 565-0871, Japan
* Corresponding author. Tel.: +81-6-6879-3154; fax: +81-6-6879-3163 sawa{at}surg1.med.osaka-u.ac.jp
Objective: Heat shock protein 72 (HSP72) is involved in the myocardial self-preservation system under several conditions such as ischemia–reperfusion injury or late preconditioning. However, its mechanism is not fully understood. Ecto-5'-nucleotidase is a key enzyme for synthesizing adenosine and plays an important role in ischemic preconditioning. In this study, we tested the hypothesis that ecto-5'-nucleotidase plays a role in the cardioprotection of HSP72. Methods: Rat hearts (H group, n=6) were transfected with HSP72 gene by an intracoronary infusion of hemagglutinating virus of Japan (HVJ)–liposome complex. Control hearts (C group, n=6) were transfected with the β-galactosidase gene. Following 30 min of normothermic ischemia, grafts were reperfused using Langendorff apparatus. Results: The activity of ecto-5'-nucleotidase was significantly higher in H group than C group both before and after ischemia–reperfusion (H vs. C; 0.51±0.05 vs. 0.29±0.06, and 1.41±0.15 vs. 0.85±0.11 nmol/mg protein/min, P<0.05). H group also showed significant better functional recoveries than C group (P<0.05), as well as less creatine phosphokinase leakage (4.4±2.8 vs. 14.2±3.4 mU/min, P<0.05) and higher adenosine release (247.5±35.1 vs. 54.3±1.7 pmol/min, P<0.05). Administration of 
,β-methylene adenosine diphosphate (AMP-CP), an inhibitor of ecto-5'-nucleotidase, significantly diminished the tolerance to ischemia–reperfusion injury in H group (P<0.05). Conclusion: These results demonstrated that ecto-5'-nucleotidase activated by an overexpression of HSP72 attenuated ischemia–reperfusion injury in the rat myocardium. They suggest that ecto-5'-nucleotidase plays a role in the cardioprotective effects of HSP72 in rat hearts.
KEYWORDS Adenosine; Gene therapy; Hypoxia/anoxia; Preconditioning; Ventricular function
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