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PLoS One. 2012;7(6):e39790. doi: 10.1371/journal.pone.0039790. Epub 2012 Jun 27.

Regression of atherosclerosis is characterized by broad changes in the plaque macrophage transcriptome.

Author information

1
Division of Cardiology, and the Marc and Ruti Bell Program in Vascular Biology, Department of Medicine, New York University School of Medicine, New York, New York, United States of America.

Abstract

We have developed a mouse model of atherosclerotic plaque regression in which an atherosclerotic aortic arch from a hyperlipidemic donor is transplanted into a normolipidemic recipient, resulting in rapid elimination of cholesterol and monocyte-derived macrophage cells (CD68+) from transplanted vessel walls. To gain a comprehensive view of the differences in gene expression patterns in macrophages associated with regressing compared with progressing atherosclerotic plaque, we compared mRNA expression patterns in CD68+ macrophages extracted from plaque in aortic aches transplanted into normolipidemic or into hyperlipidemic recipients. In CD68+ cells from regressing plaque we observed that genes associated with the contractile apparatus responsible for cellular movement (e.g. actin and myosin) were up-regulated whereas genes related to cell adhesion (e.g. cadherins, vinculin) were down-regulated. In addition, CD68+ cells from regressing plaque were characterized by enhanced expression of genes associated with an anti-inflammatory M2 macrophage phenotype, including arginase I, CD163 and the C-lectin receptor. Our analysis suggests that in regressing plaque CD68+ cells preferentially express genes that reduce cellular adhesion, enhance cellular motility, and overall act to suppress inflammation.

PMID:
22761902
PMCID:
PMC3384622
DOI:
10.1371/journal.pone.0039790
[Indexed for MEDLINE]
Free PMC Article

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