© 2000 by European Society of Cardiology
Copyright © 2000, European Society of Cardiology
Unstable angina activates myocardial heat shock protein 72, endothelial nitric oxide synthase, and transcription factors NF
B and AP-1
aCrafoord Laboratory of Experimental Surgery, Karolinska Hospital, S-171 76 Stockholm, Sweden
bCenter for Molecular Medicine, Karolinska Hospital, S-171 76 Stockholm, Sweden
cDepartment of Thoracic Surgery, Karolinska Hospital, S-171 76 Stockholm, Sweden
* Corresponding author. Tel.: +46-8-517-74846; fax: +46-8-517-73557 guro.valen{at}cmm.ki.se
Objective: Unstable angina may improve the clinical outcome of acute myocardial infarction, but increases the morbidity and mortality of open heart surgery. We hypothetized that unstable angina influences the myocardium, and investigated the expression of the inducible heat shock protein 72 (HSP72), constitutive HSP73, and endothelial nitric oxide synthase (eNOS), and activation of the transcription factors NF
B and AP-1 in cardiac tissue. Methods: Biopsies were taken from the right atrium of 15 patients with unstable and 15 with stable angina undergoing coronary artery bypass grafting. Immunoblotting with monoclonal antibodies against HSP72, HSP73, and eNOS were performed on protein extracts, while nuclear proteins were assessed by electromobility shift assay. Results: When calculating the optical density of the bands, patients with unstable angina had more than twice as much HSP72 and eNOS as stable patients (P<0.005), while HSP73 was similar in both groups. Nuclear translocation of NFB and AP-1 was found in patients with anginal pain shortly before surgery, but not in stable patients or in patients without symptoms for 4 days or more prior to surgery. Conclusions: HSP72 and eNOS, which may be associated with cardioprotection in ischemic preconditioning, are increased in atrial tissue of patients with unstable angina. Activation of NFB and AP-1, which regulate a battery of inflammatory genes, was found in hearts of unstable patients. NFB activation may induce a myocardial proinflammatory state, possibly making the unstable myocardium more susceptible to the inflammation induced by open heart surgery.
KEYWORDS Coronary disease; Endothelial factors; Hypoxia/anoxia; Infection/inflammation; Preconditioning
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