Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 117, Issue 1, Pages 195-205Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI29950
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Funding
- NATIONAL CANCER INSTITUTE [P01CA069246] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL034636, P01HL036028, U01HL080731] Funding Source: NIH RePORTER
- NCI NIH HHS [R24 CA69246, P01 CA069246] Funding Source: Medline
- NHLBI NIH HHS [P01 HL036028, U01 HL080731, R01 HL034636, R01HL034636, HL53393, HL36028] Funding Source: Medline
- PHS HHS [P01-A154904] Funding Source: Medline
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Macrophage accumulation participates decisively in the development and exacerbation of atherosclerosis. Circulating monocytes, the precursors of macrophages, display heterogeneity in mice and humans, but their relative contribution to atherogenesis remains unknown. We report here that the Ly-6C(hi) monocyte subset increased dramatically in hypercholesterolemic apoE-deficient mice consuming a high-fat diet, with the number of Ly-6C(hi) cells doubling in the blood every month. Ly-6C(hi) monocytes adhered to activated endothelium, infiltrated lesions, and became lesional macrophages. Hypercholesterolemia-associated monocytosis (HAM) developed from increased survival, continued cell proliferation, and impaired Ly-6C(hi) to Ly-6C(lo) conversion and subsided upon statin-induced cholesterol reduction. Conversely, the number of Ly-6C(lo) cells remained unaffected. Thus, we believe that Ly-6C(hi) monocytes represent a newly recognized component of the inflammatory response in experimental atherosclerosis.
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