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Enhanced neutrophil expression of annexin-1 in coronary artery disease
Örebro University, School of Health and Medical Sciences.
Linkoping Univ, Linkoping, Sweden.
Linkoping Univ, Linkoping, Sweden.
Linkoping Univ, Linkoping, Sweden.
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2010 (English)In: Metabolism: Clinical and Experimental, ISSN 0026-0495, E-ISSN 1532-8600, Vol. 59, no 3, p. 433-440Article in journal (Refereed) Published
Abstract [en]

The systemic inflammatory activity in patients with stable coronary artery disease (CAD) is associated with a dysregulated cortisol response. Moreover, an aberrant activation status of neutrophils in CAD has been discussed; and the question of glucocorticoid resistance has been raised. The anti-inflammatory actions of glucocorticoids are mediated by annexin-1 (ANXA1). We investigated the expression of glucocrticoid receptors (GR) and ANXA1, as well as the exogenous effects of ANXA1 on neutrophils in CAD patients and related the data to diurnal salivary cortisol. Salivary cortisol levels were measured in the morning and evening during 3 consecutive days in 30 CAD patients and 30 healthy individuals. The neutrophil expression of GR and ANXA1 was determined by flow cytometry. The effect of exogenous ANXA1 was determined in a neutrophil stimulation assay. The patients showed a flattened diurnal cortisol pattern compared with healthy subjects, involving higher levels in the evening. The neutrophil expression of GR-total and GR-alpha was decreased, whereas the GR-beta expression did not differ compared with controls. The neutrophil expression of ANXA1 was significantly increased in patients. Ex vivo, ANXA1 impaired the leukotriene B-4-induced neutrophil production of reactive oxygen species in patients but not in controls. Our findings indicate a persistent overactivation of the hypothalamic-pituitary-adrenal axis in CAD patients but do not give any evidence for glucocorticoid resistance, as assessed by the neutrophil expression of OR and ANXA1. The altered neutrophil phenotype in CAD may thus represent a long-term response to disease-related activation. (C) 2010 Elsevier Inc. All rights reserved.

Place, publisher, year, edition, pages
2010. Vol. 59, no 3, p. 433-440
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Medical and Health Sciences
Research subject
Medicine
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URN: urn:nbn:se:oru:diva-12974DOI: 10.1016/j.metabol.2009.07.044ISI: 000276761800021OAI: oai:DiVA.org:oru-12974DiVA, id: diva2:383082
Available from: 2011-01-04 Created: 2011-01-03 Last updated: 2018-04-23Bibliographically approved

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Särndahl, Eva

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