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(Circulation Research. 2005;97:955.)
© 2005 American Heart Association, Inc.

Editorials

Tissue-Resident Bone Marrow–Derived Progenitor Cells

Key Players in Hypoxia-Induced Angiogenesis

Gwenaele Garin, Marlene Mathews, Bradford C. Berk

From the Cardiovascular Research Institute and Department of Medicine, University of Rochester Medical Center, NY.

Correspondence to Bradford C. Berk, Department of Medicine, University of Rochester, Box MED, Rochester, NY 14642. E-mail bradford_berk@urmc.rochester.edu

See related article on pages 1027–1035

Key Words: stem cells • angiogenesis • hypoxia • bone marrow–derived cells

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Hypoxia is a common feature of many diseases, including myocardial infarction,¹ cerebral ischemia,² pulmonary hypertension,³ and cancer.⁴ Thus, understanding the role of hypoxia in the pathogenesis of ischemic disease has significant therapeutic implications. Following ischemic injury, the growth of new blood vessels, neovascularization, is critical to maintain tissue reperfusion and homeostasis. Neovascularization occurs via 2 primary mechanisms: angiogenesis, the sprouting of new vessels from preexisting resident endothelium, and vasculogenesis, the organization of progenitor cells into vascular structures. Vasculogenesis was initially defined strictly as a developmental process.⁵ However, the characterization of bone marrow–derived progenitor cells (BMCs), which are able to differentiate into vascular cells, has suggested that vasculogenesis may also occur in adults.^6,7 The remarkable ability of BMCs to contribute to vessel formation suggests a potentially beneficial role for these progenitor cells in regenerative medicine. Indeed, when BMCs are injected into animal models of ischemia, they "home" to sites of injury, migrate into tissues, and are associated with restoration of blood flow.⁸ Mobilization of BMCs has been reported to have beneficial effects after myocardial infarction^9,10 and arterial injury.¹¹ Moreover, recent clinical trials reveal promising results using BMC injection as a treatment for myocardial infarction.¹²

Previous studies have shown that BMCs are rapidly mobilized and recruited to sites of vessel injury.¹³ There is keen interest in determining which stimuli cause BMCs to home selectively to areas of ischemia. Recently, a molecular link between hypoxia and BMC mobilization has been reported involving the transcription factor hypoxia-inducible factor 1 and the chemokine stromal derived . . . [Full Text of this Article]

Related Article:

Mobilization of Bone Marrow–Derived Cells Enhances the Angiogenic Response to Hypoxia Without Transdifferentiation Into Endothelial Cells

Thomas J. O’Neill, IV, Brian R. Wamhoff, Gary K. Owens, and Thomas C. Skalak
Circ. Res. 2005 97: 1027-1035. [Abstract] [Full Text] [PDF]

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