doi: 10.1161/01.ATV.0000249623.79871.bc
© 2006 American Heart Association, Inc.
Editorials |
Origin of Neointimal Smooth Muscle
We’ve Come Full Circle
From the Department of Molecular Physiology and Biological Physics (M.H.H., J.A.T., G.K.O.) and the Department of Medicine, Cardiovascular Division (B.R.W.), University of Virginia, Charlottesville.
Correspondence to Dr Gary K. Owens, Department of Molecular Physiology and Biological Physics, University of Virginia, MR5 Room 1220, 415 Lane Road, PO Box 801394, Charlottesville, VA 22908. E-mail gko@virginia.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
The origin of smooth muscle cells (SMCs) in atherosclerotic lesions has been a hotly debated topic for more than four decades. Until recently, it was widely accepted that the majority of smooth muscle cells in atherosclerotic lesions originate from the medial layer of the vessel wall, with local SMC proliferation and migration leading to remodeling of the vessel wall and vessel lumen.1,2 Recent reports in the literature, however, claimed that SMCs in atherosclerotic lesions originate primarily from circulating bone marrow progenitor cells.3,4 Where these cells originate from is not merely academic, because the cells that give rise to SMCs within atherosclerotic lesions would likely serve as targets for current and future therapeutic interventions. The bone marrow–derived origin suggested by these articles would indicate that attempts to control SMC phenotype in in-stent restenosis, transplant atherosclerosis, or fibrous cap rupture should be targeted toward these cells from the marrow. However, we cautioned in 2004 that if anything, the bone marrow–derived intimal SMC paradigm was "Lost in Transdifferentiation",5 and further studies were needed to clearly resolve this critically important issue.
See page 2696
In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology, Bentzon and colleagues provide excellent evidence that bone marrow–derived cells do not give rise to vascular SMCs in hyperlipidemia-induced atherosclerotic plaques in the apoE knockout mouse.6 These investigators studied plaques in apoE–/– mice that had their bone marrow reconstituted from sex-mismatched apoE–/–/eGFP+ animals, and then performed meticulous high-resolution z-axis sectioning of atherosclerotic lesions induced by Western diet to
Related Article:
Arterioscler Thromb Vasc Biol 2006 26: 2696-2702.
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