Mechanism of extracellular ATP- and adenosine-induced apoptosis of cultured pulmonary artery endothelial cells.
Identifieur interne : 002719 ( Main/Exploration ); précédent : 002718; suivant : 002720Mechanism of extracellular ATP- and adenosine-induced apoptosis of cultured pulmonary artery endothelial cells.
Auteurs : S. Rounds [États-Unis] ; W L Yee ; D D Dawicki ; E. Harrington ; N. Parks ; M V CutaiaSource :
- The American journal of physiology [ 0002-9513 ] ; 1998.
Descripteurs français
- KwdFr :
- Adenosine kinase (antagonistes et inhibiteurs), Adenosylhomocysteinase, Adénosine (analogues et dérivés), Adénosine (pharmacologie), Adénosine triphosphate (pharmacologie), Animaux, Antienzymes (pharmacologie), Apoptose (), Apoptose (physiologie), Artère pulmonaire, Bovins, Cellules cultivées, Colorants fluorescents, Concentration en ions d'hydrogène, Endothélium vasculaire (), Endothélium vasculaire (cytologie), Endothélium vasculaire (physiologie), Fluorescéines, Hydrolases (antagonistes et inhibiteurs), Inhibiteurs de l'adénosine désaminase.
- MESH :
- analogues et dérivés : Adénosine.
- antagonistes et inhibiteurs : Adenosine kinase, Hydrolases.
- cytologie : Endothélium vasculaire.
- pharmacologie : Adénosine, Adénosine triphosphate, Antienzymes.
- physiologie : Apoptose, Endothélium vasculaire.
- Adenosylhomocysteinase, Animaux, Apoptose, Artère pulmonaire, Bovins, Cellules cultivées, Colorants fluorescents, Concentration en ions d'hydrogène, Endothélium vasculaire, Fluorescéines, Inhibiteurs de l'adénosine désaminase.
English descriptors
- KwdEn :
- Adenosine (analogs & derivatives), Adenosine (pharmacology), Adenosine Deaminase Inhibitors, Adenosine Kinase (antagonists & inhibitors), Adenosine Triphosphate (pharmacology), Adenosylhomocysteinase, Animals, Apoptosis (drug effects), Apoptosis (physiology), Cattle, Cells, Cultured, Endothelium, Vascular (cytology), Endothelium, Vascular (drug effects), Endothelium, Vascular (physiology), Enzyme Inhibitors (pharmacology), Fluoresceins, Fluorescent Dyes, Hydrogen-Ion Concentration, Hydrolases (antagonists & inhibitors), Pulmonary Artery, Sodium-Hydrogen Exchangers (metabolism).
- MESH :
- chemical , analogs & derivatives : Adenosine.
- chemical , antagonists & inhibitors : Adenosine Kinase, Hydrolases.
- chemical , metabolism : Sodium-Hydrogen Exchangers.
- chemical , pharmacology : Adenosine, Adenosine Triphosphate, Enzyme Inhibitors.
- chemical : Adenosine Deaminase Inhibitors, Adenosylhomocysteinase, Fluoresceins, Fluorescent Dyes.
- cytology : Endothelium, Vascular.
- drug effects : Apoptosis, Endothelium, Vascular.
- physiology : Apoptosis, Endothelium, Vascular.
- Animals, Cattle, Cells, Cultured, Hydrogen-Ion Concentration, Pulmonary Artery.
Abstract
Apoptosis may be important in the exacerbation of endothelial cell injury or limitation of endothelial cell proliferation. We have found that extracellular ATP (exATP) and adenosine cause endothelial apoptosis and that the development of apoptosis is linked to intracellular metabolism of adenosine [Dawicki, D. D., D. Chatterjee, J. Wyche, and S. Rounds. Am. J. Physiol. 273 (Lung Cell Mol. Physiol. 17): L485-L494, 1997]. In the present study, we investigated the mechanism of this effect. We found that exATP, adenosine, and the S-adenosyl-L-homocysteine (SAH) hydrolase inhibitor MDL-28842 caused apoptosis and decreased the ratio of S-adenosyl-L-methionine to SAH compared with untreated control cells. Using release of soluble [3H]thymidine as a measure of DNA fragmentation, we found that the effect of adenosine on soluble DNA release was potentiated by coincubation with homocysteine. These results suggest that the mechanism of exATP- and adenosine-induced endothelial cell apoptosis involves inhibition of SAH hydrolase. exATP-induced apoptosis was enhanced by an inhibitor of adenosine deaminase, whereas exogenous adenosine-induced apoptosis was partially inhibited by an adenosine deaminase inhibitor. These results suggest that adenosine deaminase may also be involved in the mechanism of adenosine-induced endothelial cell apoptosis. Adenosine and MDL-28842 caused intracellular acidosis as assessed with the fluorescent probe 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein. The cell-permeant base chloroquine prevented adenosine-induced acidosis but not apoptosis. Thus, although intracellular acidosis is associated with adenosine-induced apoptosis, it is not necessary for this effect. We speculate that exATP- and adenosine-induced endothelial cell apoptosis may be due to an inhibition of methyltransferase(s) activity. Purine-induced endothelial cell apoptosis may be important in limiting endothelial cell proliferation after vascular injury.
DOI: 10.1152/ajplung.1998.275.2.L379
PubMed: 9700100
Affiliations:
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Le document en format XML
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Rounds</name><affiliation wicri:level="1"><nlm:affiliation>Pulmonary and Critical Care Medicine Section, Providence Veterans Affairs Medical Center, Brown University School of Medicine, Providence, Rhode Island 02908, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Pulmonary and Critical Care Medicine Section, Providence Veterans Affairs Medical Center, Brown University School of Medicine, Providence, Rhode Island 02908</wicri:regionArea><wicri:noRegion>Rhode Island 02908</wicri:noRegion></affiliation></author><author><name sortKey="Yee, W L" sort="Yee, W L" uniqKey="Yee W" first="W L" last="Yee">W L Yee</name></author><author><name sortKey="Dawicki, D D" sort="Dawicki, D D" uniqKey="Dawicki D" first="D D" last="Dawicki">D D Dawicki</name></author><author><name sortKey="Harrington, E" sort="Harrington, E" uniqKey="Harrington E" first="E" last="Harrington">E. Harrington</name></author><author><name sortKey="Parks, N" sort="Parks, N" uniqKey="Parks N" first="N" last="Parks">N. 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Rounds</name><affiliation wicri:level="1"><nlm:affiliation>Pulmonary and Critical Care Medicine Section, Providence Veterans Affairs Medical Center, Brown University School of Medicine, Providence, Rhode Island 02908, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Pulmonary and Critical Care Medicine Section, Providence Veterans Affairs Medical Center, Brown University School of Medicine, Providence, Rhode Island 02908</wicri:regionArea><wicri:noRegion>Rhode Island 02908</wicri:noRegion></affiliation></author><author><name sortKey="Yee, W L" sort="Yee, W L" uniqKey="Yee W" first="W L" last="Yee">W L Yee</name></author><author><name sortKey="Dawicki, D D" sort="Dawicki, D D" uniqKey="Dawicki D" first="D D" last="Dawicki">D D Dawicki</name></author><author><name sortKey="Harrington, E" sort="Harrington, E" uniqKey="Harrington E" first="E" last="Harrington">E. Harrington</name></author><author><name sortKey="Parks, N" sort="Parks, N" uniqKey="Parks N" first="N" last="Parks">N. Parks</name></author><author><name sortKey="Cutaia, M V" sort="Cutaia, M V" uniqKey="Cutaia M" first="M V" last="Cutaia">M V Cutaia</name></author></analytic><series><title level="j">The American journal of physiology</title><idno type="ISSN">0002-9513</idno><imprint><date when="1998" type="published">1998</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adenosine (analogs & derivatives)</term><term>Adenosine (pharmacology)</term><term>Adenosine Deaminase Inhibitors</term><term>Adenosine Kinase (antagonists & inhibitors)</term><term>Adenosine Triphosphate (pharmacology)</term><term>Adenosylhomocysteinase</term><term>Animals</term><term>Apoptosis (drug effects)</term><term>Apoptosis (physiology)</term><term>Cattle</term><term>Cells, Cultured</term><term>Endothelium, Vascular (cytology)</term><term>Endothelium, Vascular (drug effects)</term><term>Endothelium, Vascular (physiology)</term><term>Enzyme Inhibitors (pharmacology)</term><term>Fluoresceins</term><term>Fluorescent Dyes</term><term>Hydrogen-Ion Concentration</term><term>Hydrolases (antagonists & inhibitors)</term><term>Pulmonary Artery</term><term>Sodium-Hydrogen Exchangers (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Adenosine kinase (antagonistes et inhibiteurs)</term><term>Adenosylhomocysteinase</term><term>Adénosine (analogues et dérivés)</term><term>Adénosine (pharmacologie)</term><term>Adénosine triphosphate (pharmacologie)</term><term>Animaux</term><term>Antienzymes (pharmacologie)</term><term>Apoptose ()</term><term>Apoptose (physiologie)</term><term>Artère pulmonaire</term><term>Bovins</term><term>Cellules cultivées</term><term>Colorants fluorescents</term><term>Concentration en ions d'hydrogène</term><term>Endothélium vasculaire ()</term><term>Endothélium vasculaire (cytologie)</term><term>Endothélium vasculaire (physiologie)</term><term>Fluorescéines</term><term>Hydrolases (antagonistes et inhibiteurs)</term><term>Inhibiteurs de l'adénosine désaminase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Adenosine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Adenosine Kinase</term><term>Hydrolases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Sodium-Hydrogen Exchangers</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Adenosine</term><term>Adenosine Triphosphate</term><term>Enzyme Inhibitors</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Adenosine Deaminase Inhibitors</term><term>Adenosylhomocysteinase</term><term>Fluoresceins</term><term>Fluorescent Dyes</term></keywords><keywords scheme="MESH" qualifier="analogues et dérivés" xml:lang="fr"><term>Adénosine</term></keywords><keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Adenosine kinase</term><term>Hydrolases</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Endothélium vasculaire</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Endothelium, Vascular</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term><term>Endothelium, Vascular</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Adénosine</term><term>Adénosine triphosphate</term><term>Antienzymes</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Apoptose</term><term>Endothélium vasculaire</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Apoptosis</term><term>Endothelium, Vascular</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cattle</term><term>Cells, Cultured</term><term>Hydrogen-Ion Concentration</term><term>Pulmonary Artery</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Adenosylhomocysteinase</term><term>Animaux</term><term>Apoptose</term><term>Artère pulmonaire</term><term>Bovins</term><term>Cellules cultivées</term><term>Colorants fluorescents</term><term>Concentration en ions d'hydrogène</term><term>Endothélium vasculaire</term><term>Fluorescéines</term><term>Inhibiteurs de l'adénosine désaminase</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Apoptosis may be important in the exacerbation of endothelial cell injury or limitation of endothelial cell proliferation. We have found that extracellular ATP (exATP) and adenosine cause endothelial apoptosis and that the development of apoptosis is linked to intracellular metabolism of adenosine [Dawicki, D. D., D. Chatterjee, J. Wyche, and S. Rounds. Am. J. Physiol. 273 (Lung Cell Mol. Physiol. 17): L485-L494, 1997]. In the present study, we investigated the mechanism of this effect. We found that exATP, adenosine, and the S-adenosyl-L-homocysteine (SAH) hydrolase inhibitor MDL-28842 caused apoptosis and decreased the ratio of S-adenosyl-L-methionine to SAH compared with untreated control cells. Using release of soluble [3H]thymidine as a measure of DNA fragmentation, we found that the effect of adenosine on soluble DNA release was potentiated by coincubation with homocysteine. These results suggest that the mechanism of exATP- and adenosine-induced endothelial cell apoptosis involves inhibition of SAH hydrolase. exATP-induced apoptosis was enhanced by an inhibitor of adenosine deaminase, whereas exogenous adenosine-induced apoptosis was partially inhibited by an adenosine deaminase inhibitor. These results suggest that adenosine deaminase may also be involved in the mechanism of adenosine-induced endothelial cell apoptosis. Adenosine and MDL-28842 caused intracellular acidosis as assessed with the fluorescent probe 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein. The cell-permeant base chloroquine prevented adenosine-induced acidosis but not apoptosis. Thus, although intracellular acidosis is associated with adenosine-induced apoptosis, it is not necessary for this effect. We speculate that exATP- and adenosine-induced endothelial cell apoptosis may be due to an inhibition of methyltransferase(s) activity. Purine-induced endothelial cell apoptosis may be important in limiting endothelial cell proliferation after vascular injury.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country></list><tree><noCountry><name sortKey="Cutaia, M V" sort="Cutaia, M V" uniqKey="Cutaia M" first="M V" last="Cutaia">M V Cutaia</name><name sortKey="Dawicki, D D" sort="Dawicki, D D" uniqKey="Dawicki D" first="D D" last="Dawicki">D D Dawicki</name><name sortKey="Harrington, E" sort="Harrington, E" uniqKey="Harrington E" first="E" last="Harrington">E. Harrington</name><name sortKey="Parks, N" sort="Parks, N" uniqKey="Parks N" first="N" last="Parks">N. Parks</name><name sortKey="Yee, W L" sort="Yee, W L" uniqKey="Yee W" first="W L" last="Yee">W L Yee</name></noCountry><country name="États-Unis"><noRegion><name sortKey="Rounds, S" sort="Rounds, S" uniqKey="Rounds S" first="S" last="Rounds">S. 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