Stem cell mobilization by hyperbaric oxygen

Article (PDF Available)inAJP Heart and Circulatory Physiology 290(4):H1378-86 · May 2006with34 Reads
DOI: 10.1152/ajpheart.00888.2005 · Source: PubMed
Abstract
We hypothesized that exposure to hyperbaric oxygen (HBO(2)) would mobilize stem/progenitor cells from the bone marrow by a nitric oxide (*NO) -dependent mechanism. The population of CD34(+) cells in the peripheral circulation of humans doubled in response to a single exposure to 2.0 atmospheres absolute (ATA) O(2) for 2 h. Over a course of 20 treatments, circulating CD34(+) cells increased eightfold, although the overall circulating white cell count was not significantly increased. The number of colony-forming cells (CFCs) increased from 16 +/- 2 to 26 +/- 3 CFCs/100,000 monocytes plated. Elevations in CFCs were entirely due to the CD34(+) subpopulation, but increased cell growth only occurred in samples obtained immediately posttreatment. A high proportion of progeny cells express receptors for vascular endothelial growth factor-2 and for stromal-derived growth factor. In mice, HBO(2) increased circulating stem cell factor by 50%, increased the number of circulating cells expressing stem cell antigen-1 and CD34 by 3.4-fold, and doubled the number of CFCs. Bone marrow *NO concentration increased by 1,008 +/- 255 nM in association with HBO(2). Stem cell mobilization did not occur in knockout mice lacking genes for endothelial *NO synthase. Moreover, pretreatment of wild-type mice with a *NO synthase inhibitor prevented the HBO(2)-induced elevation in stem cell factor and circulating stem cells. We conclude that HBO(2) mobilizes stem/progenitor cells by stimulating *NO synthesis.

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Available from: Lee J Goldstein
    • "In the past 10 years, reports of increased circulating endothelial progenitor cells in mouse [21] and humans [22] have shed light on mechanisms stimulated by HBO 2 for wound healing and angiogenesis [23]. In humans and mice, the process of increased stem cell release is a nitric oxide (NO@BULLET) mediated process that is triggered by HBO 2 . "
    [Show abstract] [Hide abstract] ABSTRACT: The current debate surrounding the use of hyperbaric oxygen (HBO2) for neurological indications, specifically mild to moderate chronic traumatic brain injury (mTBI) and post-concussion syndrome (PCS), is mired in confusion due to the use of non-validated controls and an unfamiliarity by many practitioners of HBO2 therapy with the experimental literature. In the past 40 years, the use of an air sham (21% oxygen, 1.14-1.5 atmospheres absolute/atm abs) in clinical and animal studies, instead of observational or crossover controls, has led to false acceptance of the null hypothesis (declaring no effect when one is present), due to the biological activity of these “sham” controls. The recent Department of Defense/Veterans Administration (DoD/VA) sponsored trials, previous published reports on the use of HBO2 therapy on strokeand mTBI and preliminary reports from the HOPPS Army trial, have helped to highlight the biological activity of pressurized air, validate the development of a convincing control for future studies and demonstrate the effectiveness of a hyperbaric intervention for mTBI/PCS. Approval of HBO2 for neurological indications, especially for mTBI/PCS, should be granted at the federal, state and certifying body levels as a safe and viable treatment for recovery in the post-acute phase.
    Full-text · Article · Aug 2015
    • "Since 1973, hyperbaric oxygen has been used in treatment of osteoradionecrosis of the mandible (Mainous and Hart, 1975 ) and as an adjunctive therapy for chronic osteomyelitis of the jaw and jaw osteoradionecrosis (Feldmeier, 2003). Its use has a beneficial effect in the healing process due to its antimicrobial action (Knighton et al, 1984Knighton et al, , 1990), while some studies show that hyperbaric oxygen enhances mobilization of stem cells (Thom et al, 2006), angiogenesis (Gallagher et al, 2006) and processes critical to wound healing of tissues (Tandara and Mustoe, 2004; Asano et al, 2007; Boykin and Baylis, 2007). One role of hyperbaric oxygen in resolution of osteonecrotic lesions is the increase of partial pressure of oxygen (PO2) in tissues, resulting in (i) increased diffusion of oxygen into tissues and subsequent beneficial outcomes of this action and (ii) local increase of concentrations of RNS (reactive nitrogen species) and ROS (reactive oxygen species ) which influence signaling pathways, important in the healing process as well as in bone metabolism, through their action on osteoclast differentiation (Lee et al, 2005). "
    [Show abstract] [Hide abstract] ABSTRACT: Osteonecrosis of the jaw (ONJ) is a serious side effect of bisphosphonate use in patients with osteoporosis, Paget's disease, hypercalcemia of malignancy, metastatic bone disease and multiple myeloma, although recently this complication has also been reported in patients under non-bisphosphonate medication, such as denosumab and bevacizumab. The occurrence of ONJ is higher in oncology patients treated with high-dose iv bisphosphonates than in osteoporosis patients treated with oral bisphosphonates. Although multiple hypotheses have been proposed, the exact pathogenic mechanism of ONJ still remains unclear. Since treatment protocols based on randomized controlled trials (RCTs) do not exist, we critically reviewed the existing data concerning the management of bisphosphonate-related osteonecrosis of the jaw, including the most recent data for the use of teriparatide and hyperbaric oxygen. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Article · Mar 2015
    • "Historically, the beneficial effects of HBO have been attributed to the establishment of a favorable oxygen gradients [45] [46]. Recent research has revealed that HBO also generates reactive oxygen species (ROS) and reactive nitrogen species (RNS) that affect signaling processes critical to wound healing [47][54] and have shown that HBO-derived ROS and RNS induce stem cell mobilization [50] [55] [56], vasculogenesis [51] [52] [57] [58], mitochondrial biogenesis [53], and preconditioning [59][62]. Because ROS and RNS are the basis for HBO's effects on signaling, its clinical consequences in any therapeutic situation will be dose-, tissue-, and time-specific. "
    Full-text · Article · Jan 2015
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