Cdkn2a Is an Atherosclerosis Modifier Locus That Regulates Monocyte/Macrophage Proliferation
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Objective—: Common genetic variants in a 58-kb region of chromosome 9p21, near the CDKN2A/CDKN2B tumor suppressor locus, are strongly associated with coronary artery disease. However, the underlying mechanism of action remains unknown. Methods and Results—: We previously reported a congenic mouse model harboring an atherosclerosis susceptibility locus and the region of homology with the human 9p21 locus. Microarray and transcript-specific expression analyses showed markedly decreased Cdkn2a expression, including both p16 INK4a and p19 ARF , but not Cdkn2b ( p15 INK4b ), in macrophages derived from congenic mice compared with controls. Atherosclerosis studies in subcongenic strains revealed genetic complexity and narrowed 1 locus to a small interval including Cdkn2a/b . Bone marrow (BM) transplantation studies implicated myeloid lineage cells as the culprit cell type, rather than resident vascular cells. To directly test the role of BM-derived Cdkn2a transcripts in atherogenesis and inflammatory cell proliferation, we performed a transplantation study using Cdkn2a +/− cells in the Ldlr −/− mouse model. Cdkn2a -deficient BM recipients exhibited accelerated atherosclerosis, increased Ly6C hi proinflammatory monocytes, and increased monocyte/macrophage proliferation compared with controls. Conclusion—: These data provide a plausible mechanism for accelerated atherogenesis in susceptible congenic mice, involving decreased expression of Cdkn2a and increased proliferation of monocyte/macrophages, with possible relevance to the 9p21 human locus.
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Knock-out of p16 INK4a, p19 ARF, p21, and p53 had a pro-atherosclerotic effect in mice.
“Knock-out of p16 INK4a, p19 ARF, p21, and p53 had a pro-atherosclerotic effect in mice.203–205”
From Senescence-induced inflammation: an important player and key therapeutic target in atherosclerosis (2020) · cites this paper as [203]
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- Authors
- Kuo, C.-L., Murphy, A. J., Sayers, S., Li, R., Yvan-Charvet, L., Davis, J. Z., Krishnamurthy, J., Liu, Y., Puig, O., Sharpless, N. E., Tall, A. R., & Welch, C. L.
- Affiliations
- University of North Carolina at Chapel Hill (US)
- From the Division of Molecular Medicine, Department of Medicine, Columbia University, New York, NY (C.-L.K., A.J.M., S.S., R.L., L.Y.-C., J.Z.D., A.R.T., C.L.W.); Institute of Human Nutrition, Columbia University Medical Center, New York, NY (C.-L.K.); Department of Medicine and Genetics and the Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, NC (J.K., Y.L., N.E.S.); Molecular Profiling Research Informatics, Merck Research Laboratories, Rahway,...
- Corresponding author
- Welch, Carrie L.
- Venue
- Arteriosclerosis, Thrombosis, and Vascular Biology
- Published
- 2011-11
- Volume
- 31
- Issue
- 11
- Pages
- 2483-2492
- ISSN
- 1079-5642 (ISSN-L)
- 1524-4636
- PMC
- PMC3350106
- OpenAlex
- W2168306321
- Cited by
- 73
- References
- 52
- Citations by year
- 2026: 5 · 2025: 3 · 2024: 5 · 2023: 4 · 2022: 2 · 2021: 2 · 2020: 1 · 2019: 7 · 2018: 4 · 2017: 4 · 2016: 6 · 2015: 3 · 2014: 7 · 2013: 8 · 2012: 11
- FWCI
- 3.83
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Arteriosclerosis Thrombosis and Vascular Biology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Wellcome Trust
- National Institutes of Health (5r01ag024379-15)
- National Institute on Aging (AG024379, R01-AG024379)
- National Heart, Lung, and Blood Institute (R01HL102206, P01HL054591, HL 54591)
- National Institute of Environmental Health Sciences (P30ES010126)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Cerebrovascular and Carotid Artery Diseases
- Keywords
- CDKN2A, CDKN2B, 9p21, atherosclerosis, coronary artery disease, p16INK4a, p19ARF, congenic mice, bone marrow transplantation, Ly6C+ monocytes, atherogenesis, genetic susceptibility loci
- MeSH terms
- Animals, Disease Models, Animal, Macrophages, Monocytes, Receptors, LDL, Bone Marrow Transplantation, Mice, Knockout, Cyclin-Dependent Kinase Inhibitor p16, Genes, p16, Genetic Predisposition to Disease, Mice, Congenic, Cell Proliferation, Atherosclerosis, Mice
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