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Regression of Atherosclerosis Is Characterized by Broad Changes in the Plaque Macrophage Transcriptome
Open accessAbstract
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.
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“Indeed, lipid-lowering interventions in atherosclerotic mice seem both to attenuate lipoprotein modification in the arterial wall and to promote a pro-resolving phenotype in lesional macrophages, all of which precede plaque regression209.”
From Inflammation and its resolution in atherosclerosis: mediators and therapeutic opportunities (2019) · cites this paper as [209]
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Metadata
- Authors
- Feig, J. E., Vengrenyuk, Y., Reiser, V., Wu, C., Statnikov, A., Aliferis, C. F., Garabedian, M. J., Fisher, E. A., & Puig, O.
- Affiliations
- New York University (US)
- Corresponding author
- Fisher, Edward A.
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2012-06-27
- Volume
- 7
- Issue
- 6
- Pages
- e39790
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC3384622
- OpenAlex
- W2167104273
- Cited by
- 118
- References
- 38
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 7 · 2023: 3 · 2022: 7 · 2021: 9 · 2020: 10 · 2019: 13 · 2018: 14 · 2017: 6 · 2016: 4 · 2015: 14 · 2014: 16 · 2013: 8 · 2012: 2
- FWCI
- 5.57
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Figshare (submittedVersion, cc-by)
- Funders
- National Institutes of Health
- National Institute on Aging (AG-029748, F30AG029748)
- National Heart, Lung, and Blood Institute (R01HL084312, HL-084312, T32HL098129)
- U.S. National Library of Medicine (R56LM007948)
- National Center for Research Resources (UL1RR029893)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cerebrovascular and Carotid Artery Diseases
- Keywords
- atherosclerosis regression, atherosclerotic plaque, macrophages, macrophage transcriptome, CD68+ macrophages, M2 macrophage phenotype, anti-inflammatory macrophages, cell motility, cell adhesion, arginase-1, CD163, hyperlipidemia, plaque regression
- MeSH terms
- CD68 Molecule, Animals, Apolipoproteins E, Macrophages, Mice, Inbred C57BL, Antigens, Differentiation, Myelomonocytic, Antigens, CD, Mice, Knockout, Atherosclerosis, Mice, Transcriptome, Real-Time Polymerase Chain Reaction
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