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Circulation. 2003;108:457-463
Published online before print July 14, 2003, doi: 10.1161/01.CIR.0000082924.75945.48
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(Circulation. 2003;108:457.)
© 2003 American Heart Association, Inc.


Basic Science Reports

Aging, Progenitor Cell Exhaustion, and Atherosclerosis

Frederick M. Rauscher, MD; Pascal J. Goldschmidt-Clermont, MD; Bryce H. Davis, BSE*; Tao Wang, MD, PhD*; David Gregg, MD; Priya Ramaswami, BE; Anne M. Pippen, BS; Brian H. Annex, MD; Chunming Dong, MD; Doris A. Taylor, PhD

From the Division of Cardiology, Department of Medicine, Duke University Medical Center, Durham, NC.

Correspondence to Pascal J. Goldschmidt-Clermont, MD, and Doris A. Taylor, PhD, Department of Medicine, Duke University Medical Center, Box 3845, Durham, NC 27710. E-mail pascal.goldschmidt{at}duke.edu or dataylor@duke.edu

Received April 22, 2003; de novo received May 30, 2003; accepted June 11, 2003.

Background— Atherosclerosis is largely attributed to chronic vascular injury, as occurs with excess cholesterol; however, the effect of concomitant vascular aging remains unexplained. We hypothesize that the effect of time in atherosclerosis progression is related to obsolescence of endogenous progenitor cells that normally repair and rejuvenate the arteries.

Methods and Results— Here we show that chronic treatment with bone marrow–derived progenitor cells from young nonatherosclerotic ApoE-/- mice prevents atherosclerosis progression in ApoE-/- recipients despite persistent hypercholesterolemia. In contrast, treatment with bone marrow cells from older ApoE-/- mice with atherosclerosis is much less effective. Cells with vascular progenitor potential are decreased in the bone marrow of aging ApoE-/- mice, but cells injected from donor mice engraft on recipient arteries in areas at risk for atherosclerotic injury.

Conclusions— Our data indicate that progressive progenitor cell deficits may contribute to the development of atherosclerosis.


Key Words: aging • atherosclerosis • stem cells


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