Circulating levels of MCP-1 and eotaxin are not associated with presence of atherosclerosis or previous myocardial infarction.

Abstract:

:The chemokines are a family of signalling proteins that participate in regulation of the immune system and have been implicated in the pathogenesis of vascular diseases. Deleting the gene encoding the chemokine MCP-1 in mouse models of atherosclerosis reduces lipid lesion formation and circulating chemokines are upregulated in man immediately following myocardial infarction (MI) or coronary angioplasty. We have therefore investigated whether circulating levels of two chemokines (MCP-1 and eotaxin) differ between subjects with and without atherosclerosis. We have used three different methods of measuring the presence and extent of atherosclerosis in human subjects: duplex ultrasonography of the carotid arteries and clinical diagnosis of coronary heart disease on individuals from the general population and coronary angiography on patients with suspected heart disease. There was no difference in the levels of circulating MCP-1 or eotaxin, measured by ELISA, between subjects with and without atherosclerosis. Furthermore, any increase in circulating MCP-1 following acute MI must be short-lived, since chemokine levels were not different in subjects who had had an MI previously compared to those who had not. We conclude that although there may be a transient increase in circulating chemokine levels following coronary angioplasty, there is no difference in the levels of circulating MCP-1 or eotaxin in subjects with and without atherosclerosis.

journal_name

Atherosclerosis

journal_title

Atherosclerosis

authors

Mosedale DE,Smith DJ,Aitken S,Schofield PM,Clarke SC,McNab D,Goddard H,Gale CR,Martyn CN,Bethell HW,Barnard C,Hayns S,Nugent C,Panicker A,Grainger DJ

doi

10.1016/j.atherosclerosis.2004.11.028

keywords:

subject

Has Abstract

pub_date

2005-12-01 00:00:00

pages

268-74

issue

2

eissn

0021-9150

issn

1879-1484

pii

S0021-9150(05)00235-2

journal_volume

183

pub_type

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