Faculty Opinions recommendation of In vivo cellular imaging pinpoints the role of reactive oxygen species in the early steps of adult hematopoietic reconstitution.

2010 ◽  
Author(s):  
Thalia Papayannopoulou ◽  
Halvard Bönig
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Cellular Imaging ◽  
Oxygen Species ◽  
Hematopoietic Reconstitution

In vivo cellular imaging pinpoints the role of reactive oxygen species in the early steps of adult hematopoietic reconstitution

Blood ◽  
2010 ◽  
Vol 115 (3) ◽  
pp. 443-452 ◽  
Author(s):  
Daniel Lewandowski ◽  
Vilma Barroca ◽  
Frédéric Ducongé ◽  
Jan Bayer ◽  
Jeanne Tran Van Nhieu ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Endothelial Cells ◽  
Femoral Head ◽  
Fiber Optic ◽  
Imaging System ◽  
Hematopoietic Cells ◽  
Oxygen Species ◽  
Hematopoietic Reconstitution

Abstract Few techniques are available to characterize in vivo the early cellular dynamics of long-term reconstitution of hematopoiesis after transplantation of hematopoietic stem cells (HSCs) after lethal irradiation. Using a fiber-optic imaging system, we track the early steps of in vivo recruitment and proliferation of Lin−Sca-1+c-Kit+CD34− (LSKCD34−) HSCs highly enriched in HSCs and transplanted into lethally irradiated mice. Recruitment of the transplanted LSKCD34− hematopoietic cells first occurs in the femoral head and is continuous during 24 hours. Quantification of the fluorescence emitted by the transplanted hematopoietic cells shows that proliferation of LSKCD34− hematopoietic cells in the femoral head was potent 3 days after transplantation. Using a development of this fiber-optic imaging system, we show that the transplanted LSKCD34− hematopoietic cells are associated with vascularized structures as early as 5 hours after transplantation. This early association is dependent on reactive oxygen species (ROS) partly through the regulation of vascular cell adhesion molecule-1 expression on endothelial cells and is followed by a ROS-dependent proliferation of LSKCD34− hematopoietic cells. This new in vivo imaging technique permits the observation of the early steps of hematopoietic reconstitution by HSCs in long bones and shows a new role of ROS in the recruitment of HSCs by bone marrow endothelial cells.

In Vivo Cellular Imaging Pinpoints the Role of Reactive Oxygen Species in the Early Steps of Adult Hematopoietic Reconstitution

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 2454-2454
Author(s):  
Daniel Lewandowski ◽  
Vilma Barroca ◽  
Frédéric Ducongé ◽  
Bertrand Tavitian ◽  
Paul-Henri Roméo
Keyword(s):  
Reactive Oxygen Species ◽  
Stem Cells ◽  
Imaging System ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Somatic Stem Cells ◽  
Cellular Dynamics ◽  
Hematopoietic Reconstitution ◽  
Lethal Irradiation

Abstract Progress in regenerative medicine will be greatly helped by the characterization of the in vivo processes that lead to tissue reconstitution by adult somatic stem cells. Many major advances have been achieved in the purification and the ex vivo amplification of the adult somatic stem cells, but very few data are available on the pre-requisites that will enhance their in vivo biological activities. The best studied model of tissue reconstitution is the long-term reconstitution of hematopoiesis after transplantation of adult hematopoietic stem cells (HSCs) following lethal irradiation and imaging strategies are amongst the most promising techniques to reveal the in vivo cellular dynamics of this process. Here, we present a new imaging technique to track labeled cells in living animals and we show that this technique can visualize the hematopoietic reconstitution within the femoral cavity after lethal irradiation. We use a fibered in vivo confocal fluorescence imaging system that can navigate inside the femoral cavity from the knee to the femoral head. Imaging is done in living mice, does not alter their viability, does not interfere with hematopoietic reconstitution and can easily be used to follow the temporal dynamics of tissue reconstitution in the mouse at a cellular level. Using this imaging system, we track the temporal and topological cellular dynamics of in vivo engraftment and proliferation of Lin-Sca+c−Kit+CD34− cells (LSKCD34−), enriched in HSCs, transplanted into lethally irradiated mice. Homing and engraftment of LSKCD34− hematopoietic cells first occur in the two femoral epiphyses where these cells are found associated with vascularized structures as early as one hour after transplantation. Reactive oxygen species (ROS) regulate the initial homing of transplanted HSCs through the modulation of VCAM-1 expression by the endothelial cells and the proliferation of transplanted HSCs.

The Role of Reactive Oxygen Species in the Light-Induced Deformation of DNA

1984 ◽  
Vol 39 (9) ◽  
pp. 1276-1280 ◽  
Author(s):  
R. Baumann ◽  
M. Herrmann ◽  
H. Parlar
Keyword(s):  
Reactive Oxygen Species ◽  
Excited States ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
In Vivo Experiments ◽  
Pyrimidine Bases ◽  
Effect Of Oxygen

Dimerizations and reactions with water of pyrimidine bases are the primary steps held respon­sible for the deformation of DNA at short wavelengths in vitro and in vivo experiments. However the influence of oxygen in combination with water on the UV deformation at wavelengths rep­resentative for troposphere is evident from the observed data and both together are needed to change the DNA structure. The only plausible explanation for the effect of oxygen is the forma­tion of reactive oxygen species during the UV irradiation of DNA. In the present work the deformation of DNA by different oxygen species like singlet oxygen (1O2), superoxideanion (O2-), hydroxyradical (·OH), ozone (O3) and hydrogenperoxide (H2O2) is excluded with the help of chemical-trapping experiments. The photo-induced transformation proceeds via excited states of DNA. which react with groundstate oxygen to afford peroxide.

Nitrate tolerance does not increase production of peroxynitrite in the heart

2002 ◽  
Vol 283 (1) ◽  
pp. H69-H76 ◽  
Author(s):  
Tamás Csont ◽  
Csaba Csonka ◽  
Annamária Ónody ◽  
Anikó Görbe ◽  
László Dux ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Vascular Dysfunction ◽  
Reactive Oxygen ◽  
Nitrate Tolerance ◽  
Oxygen Species ◽  
Mechanical Function ◽  
Nitrate Treatment

Clinical studies have suggested that long-term nitrate treatment does not improve and may even worsen cardiovascular mortality, and the possible role of nitrate tolerance has been suspected. Nitrate tolerance has been recently shown to increase vascular superoxide and peroxynitrite production leading to vascular dysfunction. Nevertheless, nitrates exert direct cardiac effects independent from their vascular actions. Therefore, we investigated whether in vivo nitroglycerin treatment leading to vascular nitrate tolerance increases cardiac formation of nitric oxide (NO), reactive oxygen species, and peroxynitrite, thereby leading to cardiac dysfunction. Nitrate tolerance increased bioavailability of NO in the heart without increasing formation of reactive oxygen species. Despite elevated myocardial NO, neither cardiac markers of peroxynitrite formation nor cardiac mechanical function were affected by nitroglycerin treatment. However, serum free nitrotyrosine, a marker for systemic peroxynitrite formation, was significantly elevated in nitroglycerin-treated animals. This is the first demonstration that, although the systemic effects of nitroglycerin may be deleterious due to enhancement of extracardiac peroxynitrite formation, nitroglycerin does not result in oxidative damage in the heart.

scholarly journals Attenuation of Ischemia-Induced Mouse Brain Injury by SAG, a Redox-Inducible Antioxidant Protein

2001 ◽  
Vol 21 (6) ◽  
pp. 722-733 ◽  
Author(s):  
Guo-Yuan Yang ◽  
Li Pang ◽  
Hai-Liang Ge ◽  
Mingjia Tan ◽  
Wen Ye ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Brain Injury ◽  
Mouse Brain ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Model Systems ◽  
Oxygen Species ◽  
Antioxidant Protein

Cerebral ischemia resulting from a disruption of blood flow to the brain initiates a cascade of events that causes neuron death and leads to neurologic dysfunction. Reactive oxygen species are thought, at least in part, to mediate this disease process. The authors recently cloned and characterized an antioxidant protein, SAG (sensitive to apoptosis gene), that is redox inducible and protects cells from apoptosis induced by redox agents in a number of in vitro cell model systems. This study reports a neuroprotective role of SAG in ischemia/reperfusion-induced brain injury in an in vivo mouse model. SAG was expressed at a low level in brain tissue and was inducible after middle cerebral artery occlusion with peak expression at 6 to 12 hours. At the cellular level, SAG was mainly expressed in the cytoplasm of neurons and astrocytes, revealed by double immunofluorescence. An injection of recombinant adenoviral vector carrying human SAG into mouse brain produced an overexpression of SAG protein in the injected areas. Transduction of AdCMVSAG (wild-type), but not AdCMVmSAG (mutant), nor the AdCMVlacZ control, protected brain cells from ischemic brain injury, as evidenced by significant reduction of the infarct areas where SAG was highly expressed. The result suggests a rather specific protective role of SAG in the current in vivo model. Mechanistically, SAG overexpression decreased reactive oxygen species production and reduced the number of apoptotic cells in the ischemic areas. Thus, antioxidant SAG appears to protect against reactive oxygen species–induced brain damage in mice. Identification of SAG as a neuroprotective molecule could lead to potential stroke therapies.

In vivo key role of reactive oxygen species and NHE-1 activation in determining excessive cardiac hypertrophy

2011 ◽  
Vol 462 (5) ◽  
pp. 733-743 ◽  
Author(s):  
Oscar H. Cingolani ◽  
Néstor G. Pérez ◽  
Irene L. Ennis ◽  
María C. Álvarez ◽  
Susana M. Mosca ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cardiac Hypertrophy ◽  
Reactive Oxygen ◽  
Oxygen Species

scholarly journals Cytotoxic and Antitumor Activity of Sulforaphane: The Role of Reactive Oxygen Species

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Piero Sestili ◽  
Carmela Fimognari
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Target Cells ◽  
Cancer Therapies ◽  
Oxygen Species ◽  
Reactive Oxygen Species Formation ◽  
Species Formation

According to recent estimates, cancer continues to remain the second leading cause of death and is becoming the leading one in old age. Failure and high systemic toxicity of conventional cancer therapies have accelerated the identification and development of innovative preventive as well as therapeutic strategies to contrast cancer-associated morbidity and mortality. In recent years, increasing body ofin vitroandin vivostudies has underscored the cancer preventive and therapeutic efficacy of the isothiocyanate sulforaphane. In this review article, we highlight that sulforaphane cytotoxicity derives from complex, concurring, and multiple mechanisms, among which the generation of reactive oxygen species has been identified as playing a central role in promoting apoptosis and autophagy of target cells. We also discuss the site and the mechanism of reactive oxygen species’ formation by sulforaphane, the toxicological relevance of sulforaphane-formed reactive oxygen species, and the death pathways triggered by sulforaphane-derived reactive oxygen species.

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