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rdf:type | |
lifeskim:mentions | |
pubmed:dateCreated |
1999-1-28
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pubmed:abstractText |
Human microvascular endothelial cells grown on a 3-D reconstituted extracellular matrix (Matrigel) spontaneously and rapidly form a capillary network of tubular structures, thus modeling part of the angiogenic cascade. Exposure of the cells at the time of plating onto Matrigel to a brief episode of hypoxia (40-60) min and subsequent reoxygenation, significantly accelerated (up to 3-fold) the rate of tubular morphogenesis, as determined by computer-aided morphometry. This effect was not dependent on activation of PKC or upregulation/release of angiogenic growth factors. Rather, hypoxia/reoxygenation (H/R), but not hypoxia alone, caused the formation of reactive oxygen species (ROS) and the activation of the nuclear transcription factor NF kappa B, both of which were inhibited by ROS-scavengers, such as pyrollidine dithiocarbamate. Tube formation was inhibited, also under normoxic conditions, by diverse ROS antagonists in a dose-dependent fashion. Our results indicate that angiogenesis is accompanied by and/or requires generation of ROS. We hypothesize that in the clinical setting of hypoxia/reoxygenation during ischemic pre-conditioning, enhanced activation of ROS-dependent intracellular signaling may accelerate the rate of neovascularization also in vivo, thus contributing to the alleviation of certain ischemic lesions.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Collagen,
http://linkedlifedata.com/resource/pubmed/chemical/Drug Combinations,
http://linkedlifedata.com/resource/pubmed/chemical/Laminin,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase C,
http://linkedlifedata.com/resource/pubmed/chemical/Proteoglycans,
http://linkedlifedata.com/resource/pubmed/chemical/Reactive Oxygen Species,
http://linkedlifedata.com/resource/pubmed/chemical/matrigel
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pubmed:status |
MEDLINE
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pubmed:issn |
0065-2598
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
454
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
295-310
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:9889904-Cell Hypoxia,
pubmed-meshheading:9889904-Cell Respiration,
pubmed-meshheading:9889904-Cells, Cultured,
pubmed-meshheading:9889904-Collagen,
pubmed-meshheading:9889904-Drug Combinations,
pubmed-meshheading:9889904-Endothelium, Vascular,
pubmed-meshheading:9889904-Humans,
pubmed-meshheading:9889904-Kinetics,
pubmed-meshheading:9889904-Laminin,
pubmed-meshheading:9889904-Microcirculation,
pubmed-meshheading:9889904-NF-kappa B,
pubmed-meshheading:9889904-Neovascularization, Physiologic,
pubmed-meshheading:9889904-Oxygen Consumption,
pubmed-meshheading:9889904-Protein Kinase C,
pubmed-meshheading:9889904-Proteoglycans,
pubmed-meshheading:9889904-Reactive Oxygen Species,
pubmed-meshheading:9889904-Skin
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pubmed:year |
1998
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pubmed:articleTitle |
On the possible role of reactive oxygen species in angiogenesis.
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pubmed:affiliation |
Laboratory of Cell Biology, University of Wisconsin Medical School, Milwaukee 53201-0342, USA. pilelkes@facstaff.wisc.edu
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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