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Mechanism of extracellular ATP- and adenosine-induced apoptosis of cultured pulmonary artery endothelial cells

Identifieur interne : 002846 ( Main/Exploration ); précédent : 002845; suivant : 002847

Mechanism of extracellular ATP- and adenosine-induced apoptosis of cultured pulmonary artery endothelial cells

Auteurs : S. Rounds [États-Unis] ; WINNIE LIN YEE [États-Unis] ; D. D. Dawicki [États-Unis] ; E. Harrington [États-Unis] ; N. Parks [États-Unis] ; M. V. Cutaia [États-Unis]

Source :

American journal of physiology. Lung cellular and molecular physiology [ 1040-0605 ] ; 1998.

RBID : Pascal:98-0428766

Descripteurs français

Pascal (Inist)
- Artère pulmonaire, Apoptose, Azote monoxyde, Methyltransferases, Adénosine, Culture cellulaire, In vitro, Acidose, Homocystéine, Bovin, Cellule endothéliale.
Wicri :
- topic : Bovin.

English descriptors

KwdEn :
- Acidosis, Adenosine, Apoptosis, Bovine, Cell culture, Endothelial cell, In vitro, Methyltransferases, Nitric oxide, 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 ofthis 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.

Affiliations:

États-Unis

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Le document en format XML

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<term>Adenosine</term>
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<term>Cell culture</term>
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<term>In vitro</term>
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<term>Culture cellulaire</term>
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<term>Homocystéine</term>
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<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 ofthis 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 [<sup>3</sup>
H]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>
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Mechanism of extracellular ATP- and adenosine-induced apoptosis of cultured pulmonary artery endothelial cells

Mechanism of extracellular ATP- and adenosine-induced apoptosis of cultured pulmonary artery endothelial cells

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Descripteurs français

English descriptors

Abstract

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