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Angiotensin type 2 receptor is expressed in human atherosclerotic lesions.

Journal article
Authors Maria E. Johansson
Björn Fagerberg
Göran Bergström
Published in Journal of the renin-angiotensin-aldosterone system : JRAAS
Volume 9
Issue 1
Pages 17-21
ISSN 1470-3203
Publication year 2008
Published at Wallenberg Laboratory
Institute of Medicine, Department of Molecular and Clinical Medicine
Pages 17-21
Language en
Keywords Aged, Antigens, CD, analysis, Antigens, Differentiation, Myelomonocytic, analysis, Atherosclerosis, metabolism, pathology, Carotid Stenosis, metabolism, pathology, Female, Humans, Male, Middle Aged, Receptor, Angiotensin, Type 2, antagonists & inhibitors, biosynthesis
Subject categories Medical and Health Sciences


OBJECTIVE: Expression of the angiotensin type 2 receptor (AT2-receptor) occurs in many animal models of atherosclerosis. However, its expression in human plaques and its functional role remains undetermined. This study examined AT2-receptor expression in human atherosclerotic plaque and also explored its potentially important functional role in atherosclerosis. MATERIAL AND METHODS: We analysed carotid atherosclerotic plaques obtained from 14 Caucasian patients who had previously undergone endarterectomy for symptomatic carotid artery stenosis. Half of all subjects received treatment with an angiotensin receptor blocker (ARB) (n=7); the remaining subjects received no intervention in the renin-angiotensin system (n=7). Immunohistochemistry measured tissue expression of smooth muscle cells (a-actin), macrophages (CD68 antibody), collagen (picro-sirius), and AT2-receptor (AT2-receptor antibody). RESULTS: AT2-receptor expression occurred consistently in all specimens. Although cellular localisation varied, AT2-receptor expression levels correlated with macrophage levels (p<0.01). Compared to conventional treatment, ongoing ARB treatment affected neither AT2-receptor levels nor plaque composition. CONCLUSIONS: AT2-receptor is expressed in human atherosclerotic plaque. Furthermore, we detected no functionally important role of AT2-receptor expression and found no evidence that ARB treatment regulates AT2-receptor expression.

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