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

Jonathan E. Feig, Yuliya Vengrenyuk, Vladimir Reiser, Chaowei Wu, Alexander Statnikov, Constantin F. Aliferis, Michael J. Garabedian, Edward A. Fisher, Oscar Puig

Research output: Contribution to journalArticlepeer-review

72 Scopus citations

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.

Original languageEnglish (US)
Article numbere39790
JournalPloS one
Volume7
Issue number6
DOIs
StatePublished - Jun 27 2012

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