© 2000 American Heart Association, Inc.
Editorial |
Mining the Myocardium With Macrophage Drills
A Novel Mechanism for Revascularization
From the Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada.
Correspondence to Michelle P. Bendeck, Department of Laboratory Medicine and Pathobiology, University of Toronto, Medical Sciences Building, 1 King’s College Circle, Room 6217B, Toronto, Ontario M5S 1A8 Canada. E-mail michelle.bendeck@utoronto.ca
Key Words: myocardium • angiogenesis • vasculogenesis • macrophage • matrix metalloproteinases
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Introduction |
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Revascularization of the myocardium, or growing new blood vessels, has become an important therapeutic target to relieve tissue ischemia caused by vascular disease and restore cardiac function. Recent experimental and clinical investigations have established the feasibility of using recombinant proteins or gene transfer of angiogenic factors to facilitate neovascularization and augment collateral development in ischemic tissues.1 By traditional definition, the growth of new vessels occurs via angiogenesis or vasculogenesis. Angiogenesis is defined as the formation of new vessels by a process of sprouting from preexisting vessels. It is characterized by dedifferentiation of endothelial cells, dissolution of basement membranes, proliferation and migration of the cells, and reestablishment of new endothelium-lined capillary tubes. Vasculogenesis refers to the primary in situ differentiation of endothelial cells from mesodermal precursors and subsequent rearrangement into a primary capillary plexus.2 Vasculogenesis was originally thought to be restricted to embryonic development, but intriguing research over the last few years has pointed to alternative mechanisms for postnatal neovascularization.
Asahara and colleagues3 4 published studies reporting a
process that they termed postnatal vasculogenesis, involving
circulating endothelial progenitor cells (EPCs). They
isolated putative EPCs from human blood using antibodies to two
antigens that are shared by angioblasts and hematopoietic stem cells:
CD34, which is expressed by hematopoietic stem cells but is lost during
differentiation, and Flk-1, a receptor for vascular
endothelial growth factor that is expressed by early
hematopoietic stem cells and endothelial cells but
ceases to be expressed during hematopoietic differentiation. When
plated on fibronectin, the mononuclear EPCs from plasma formed
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