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First published online June 22, 2006
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2006-0010v1
24/10/2309    most recent
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Submitted on January 5, 2006
Accepted on June 15, 2006

Translational and Clinical Research

Endothelial Progenitor Cell Release into Circulation is Triggered by Hyperoxia-Induced Increases in Bone Marrow Nitric Oxide

Lee J. Goldstein 1, Katherine A. Gallagher 1, Stephen M. Bauer 1, Richard J. Bauer 1, Vijay Baireddy 1, Zhao-Jun Liu 1, Donald G. Buerk 2, Stephen R. Thom 3, Omaida C. Velazquez 1*

1 Department of Surgery, University of Pennsylvania Medical Center, Philadelphia, Pennsylvania
2 Departments of Physiology and Bioengineering, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania
3 Department of Emergency Medicine, Institute for Environmental Medicine, University of Pennsylvania Medical Center, Philadelphia, Pennsylvania

* To whom correspondence should be addressed. E-mail: omaida.velazquez{at}uphs.upenn.edu.


  Abstract

Endothelial progenitor cells (EPC) are known to contribute to wound healing but the physiologic triggers for their mobilization are often insufficient to induce complete wound healing in the presence of severe ischemia. EPC trafficking is known to be regulated by hypoxic gradients and induced by VEGF-mediated increases in bone marrow nitric oxide (NO). Hyperbaric oxygen (HBO) enhances wound healing though the mechanisms for its therapeutic effects are incompletely understood. It is known that HBO increases nitric oxide levels in perivascular tissues via stimulation of nitric oxide synthase (NOS). Here we show that HBO increases bone marrow NO in vivo thereby increasing release of EPC into circulation. These effects are inhibited by pretreatment with the NOS inhibitor L-nitroarginine methyl ester (L-NAME). HBO-mediated mobilization of EPC is associated with increased lower limb spontaneous circulatory recovery after femoral ligation and enhanced closure of ischemic wounds and these effects on limb perfusion and wound healing are also inhibited by L-NAME pretreatment. These data show that EPC mobilization into circulation is triggered by hyperoxia through induction of bone marrow NO with resulting enhancement in ischemic limb perfusion and wound healing.

Key Words. Endothelial progenitor cell, Hyperbaric oxygen, Hyperoxia, Nitric oxide, Neovascularization, Wound healing




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[Abstract] [Full Text] [PDF]


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