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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1 Pt 1
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| pubmed:dateCreated |
1997-9-3
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| pubmed:abstractText |
Two noninvasive methods, calorimetry and 31P nuclear magnetic resonance (NMR), were used to further define energy-consuming and energy-providing reactions in endothelial cells. With 31P-NMR, cellular ATP content was measured; with calorimetry, heat flux as a result of ATP turnover was measured. For these measurements, pig aortic endothelial cells were cultured on microcarrier beads and perfused in a column at constant flow rate. Pig aortic endothelial cells synthesize ATP mainly through glycolysis and, as determined by NMR, contain no phosphocreatine. In such a system, calorimetry-measured heat flux reflects rate of cellular ATP turnover. By use of inhibitors of ATP-dependent processes, the following changes in basal heat flux (231 +/- 65.5 microW/mg protein) were obtained: 18% for 2,3-butanedione monoxime (inhibitor of actomyosin-ATPase), 17% for wortmannin (inhibitor of myosin light chain kinase), 10% for cytochalasin D (inhibitor of actin polymerization), 23% for cycloheximide (inhibitor of protein synthesis), 11% for thapsigargin (inhibitor of endoplasmic reticulum Ca(2+)-ATPase), and 6% for bafilomycin A1 (inhibitor of lysosomal H(+)-ATPase). Cytochalasin D, 2,3-butanedione monoxime, wortmannin, and thapsigargin caused changes in F-actin distribution, as revealed by rhodamine-phalloidin cytochemistry. In a separate experimental series, when cells were perfused with a medium containing no glucose, heat flux decreased by 40% while cellular ATP remained unchanged. Inhibition of glycolysis with 2-deoxy-D-glucose decreased heat flux by 73%, and ATP was no longer visible with 31P-NMR. Despite this massive ATP depletion, which was maintained for 3 h, cells fully recovered heat flux and ATP when 2-deoxy-D-glucose was removed. The results, together with previously published data for Na(+)-K(+)-ATPase [M. L. H. Gruwel, C. Alves, and J. Schrader. Am. J. Physiol. 268 (Heart Circ. Physiol. 37): H351-H358, 1995], demonstrate that > 70% of total ATP-consuming processes of endothelial cells can be attributed to specific cellular processes. Actomyosin-ATPase (18%) and protein synthesis (23%) comprise the largest fraction. At least three-fourths of ATP synthesized is provided by glycolysis. Endothelial cells exhibit the remarkable ability to coordinate downregulation of ATP synthesis and consumption when glycolysis is inhibited.
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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/Actins,
http://linkedlifedata.com/resource/pubmed/chemical/Adenosine Triphosphatases,
http://linkedlifedata.com/resource/pubmed/chemical/Adenosine Triphosphate,
http://linkedlifedata.com/resource/pubmed/chemical/Androstadienes,
http://linkedlifedata.com/resource/pubmed/chemical/Antimycin A,
http://linkedlifedata.com/resource/pubmed/chemical/Cycloheximide,
http://linkedlifedata.com/resource/pubmed/chemical/Cytochalasin D,
http://linkedlifedata.com/resource/pubmed/chemical/Deoxyglucose,
http://linkedlifedata.com/resource/pubmed/chemical/Diacetyl,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphorus,
http://linkedlifedata.com/resource/pubmed/chemical/Thapsigargin,
http://linkedlifedata.com/resource/pubmed/chemical/diacetylmonoxime,
http://linkedlifedata.com/resource/pubmed/chemical/wortmannin
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| pubmed:status |
MEDLINE
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| pubmed:month |
Jul
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| pubmed:issn |
0002-9513
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
273
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
C205-13
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| pubmed:dateRevised |
2006-11-15
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| pubmed:meshHeading |
pubmed-meshheading:9252458-Actins,
pubmed-meshheading:9252458-Adenosine Triphosphatases,
pubmed-meshheading:9252458-Adenosine Triphosphate,
pubmed-meshheading:9252458-Androstadienes,
pubmed-meshheading:9252458-Animals,
pubmed-meshheading:9252458-Antimycin A,
pubmed-meshheading:9252458-Aorta,
pubmed-meshheading:9252458-Cells, Cultured,
pubmed-meshheading:9252458-Cycloheximide,
pubmed-meshheading:9252458-Cytochalasin D,
pubmed-meshheading:9252458-Deoxyglucose,
pubmed-meshheading:9252458-Diacetyl,
pubmed-meshheading:9252458-Endothelium, Vascular,
pubmed-meshheading:9252458-Energy Metabolism,
pubmed-meshheading:9252458-Enzyme Inhibitors,
pubmed-meshheading:9252458-Glycolysis,
pubmed-meshheading:9252458-Kinetics,
pubmed-meshheading:9252458-Magnetic Resonance Spectroscopy,
pubmed-meshheading:9252458-Phosphorus,
pubmed-meshheading:9252458-Swine,
pubmed-meshheading:9252458-Thapsigargin
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| pubmed:year |
1997
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| pubmed:articleTitle |
Energy turnover of vascular endothelial cells.
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| pubmed:affiliation |
Institut für Herz- und Kreislaufphysiologie, Heinrich Heine Universität Düsseldorf, Germany.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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