Stimulation of nucleoside efflux and inhibition of adenosine kinase by A1 adenosine receptor activation.
Identifieur interne : 001548 ( PubMed/Checkpoint ); précédent : 001547; suivant : 001549Stimulation of nucleoside efflux and inhibition of adenosine kinase by A1 adenosine receptor activation.
Auteurs : C J Sinclair [Canada] ; P N Shepel ; J D Geiger ; F E ParkinsonSource :
- Biochemical pharmacology [ 0006-2952 ] ; 2000.
English descriptors
- KwdEn :
- MESH :
- chemical , antagonists & inhibitors : Adenosine Kinase.
- chemical , metabolism : Adenosine, Carrier Proteins, Membrane Proteins, Receptors, Purinergic P1.
- Animals, Biological Transport, Cricetinae, Nucleoside Transport Proteins, Tumor Cells, Cultured.
Abstract
Adenosine is produced intracellularly during conditions of metabolic stress and is an endogenous agonist for four subtypes of G-protein linked receptors. Nucleoside transporters are membrane-bound carrier proteins that transfer adenosine, and other nucleosides, across biological membranes. We investigated whether adenosine receptor activation could modulate transporter-mediated adenosine efflux from metabolically stressed cells. DDT1 MF-2 smooth muscle cells were incubated with 10 microM [3H]adenine to label adenine nucleotide pools. Metabolic stress with the glycolytic inhibitor iodoacetic acid (1AA, 5 mM) increased tritium release by 63% (P < 0.01), relative to cells treated with buffer alone. The IAA-induced increase was blocked by the nucleoside transport inhibitor nitrobenzylthioinosine (1 microM), indicating that the increased tritium release was primarily a purine nucleoside. HPLC verified this to be [3H]adenosine. The adenosine A1 receptor selective agonist N6-cyclohexyladenosine (CHA, 300 nM) increased the release of [3H]purine nucleoside induced by IAA treatment by 39% (P < 0.05). This increase was blocked by the A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (10 microM). Treatment of cells with UTP (100 microM), histamine (100 microM), or phorbol-12-myristate-13-acetate (PMA, 10 microM) also increased [3H]purine nucleoside release. The protein kinase C inhibitor chelerythrine chloride (500 nM) inhibited the increase in [3H]purine nucleoside efflux induced by CHA or PMA treatment. The adenosine kinase activity of cells treated with CHA or PMA was found to be decreased significantly compared with buffer-treated cells. These data indicated that adenosine A1 receptor activation increased nucleoside efflux from metabolically stressed DDT1 MF-2 cells by a PKC-dependent inhibition of adenosine kinase activity.
PubMed: 10660114
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Stimulation of nucleoside efflux and inhibition of adenosine kinase by A1 adenosine receptor activation.</title><author><name sortKey="Sinclair, C J" sort="Sinclair, C J" uniqKey="Sinclair C" first="C J" last="Sinclair">C J Sinclair</name><affiliation wicri:level="4"><nlm:affiliation>Department of Pharmacology and Therapeutics, University of Manitoba, Winnipeg, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Pharmacology and Therapeutics, University of Manitoba, Winnipeg</wicri:regionArea><orgName type="university">Université du Manitoba</orgName><placeName><settlement type="city">Winnipeg</settlement><region type="state">Manitoba</region></placeName></affiliation></author><author><name sortKey="Shepel, P N" sort="Shepel, P N" uniqKey="Shepel P" first="P N" last="Shepel">P N Shepel</name></author><author><name sortKey="Geiger, J D" sort="Geiger, J D" uniqKey="Geiger J" first="J D" last="Geiger">J D Geiger</name></author><author><name sortKey="Parkinson, F E" sort="Parkinson, F E" uniqKey="Parkinson F" first="F E" last="Parkinson">F E Parkinson</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2000">2000</date><idno type="RBID">pubmed:10660114</idno><idno type="pmid">10660114</idno><idno type="wicri:Area/PubMed/Corpus">001655</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001655</idno><idno type="wicri:Area/PubMed/Curation">001655</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">001655</idno><idno type="wicri:Area/PubMed/Checkpoint">001655</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">001655</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Stimulation of nucleoside efflux and inhibition of adenosine kinase by A1 adenosine receptor activation.</title><author><name sortKey="Sinclair, C J" sort="Sinclair, C J" uniqKey="Sinclair C" first="C J" last="Sinclair">C J Sinclair</name><affiliation wicri:level="4"><nlm:affiliation>Department of Pharmacology and Therapeutics, University of Manitoba, Winnipeg, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Pharmacology and Therapeutics, University of Manitoba, Winnipeg</wicri:regionArea><orgName type="university">Université du Manitoba</orgName><placeName><settlement type="city">Winnipeg</settlement><region type="state">Manitoba</region></placeName></affiliation></author><author><name sortKey="Shepel, P N" sort="Shepel, P N" uniqKey="Shepel P" first="P N" last="Shepel">P N Shepel</name></author><author><name sortKey="Geiger, J D" sort="Geiger, J D" uniqKey="Geiger J" first="J D" last="Geiger">J D Geiger</name></author><author><name sortKey="Parkinson, F E" sort="Parkinson, F E" uniqKey="Parkinson F" first="F E" last="Parkinson">F E Parkinson</name></author></analytic><series><title level="j">Biochemical pharmacology</title><idno type="ISSN">0006-2952</idno><imprint><date when="2000" type="published">2000</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adenosine (metabolism)</term><term>Adenosine Kinase (antagonists & inhibitors)</term><term>Animals</term><term>Biological Transport</term><term>Carrier Proteins (metabolism)</term><term>Cricetinae</term><term>Membrane Proteins (metabolism)</term><term>Nucleoside Transport Proteins</term><term>Receptors, Purinergic P1 (metabolism)</term><term>Tumor Cells, Cultured</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Adenosine Kinase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Adenosine</term><term>Carrier Proteins</term><term>Membrane Proteins</term><term>Receptors, Purinergic P1</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Biological Transport</term><term>Cricetinae</term><term>Nucleoside Transport Proteins</term><term>Tumor Cells, Cultured</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Adenosine is produced intracellularly during conditions of metabolic stress and is an endogenous agonist for four subtypes of G-protein linked receptors. Nucleoside transporters are membrane-bound carrier proteins that transfer adenosine, and other nucleosides, across biological membranes. We investigated whether adenosine receptor activation could modulate transporter-mediated adenosine efflux from metabolically stressed cells. DDT1 MF-2 smooth muscle cells were incubated with 10 microM [3H]adenine to label adenine nucleotide pools. Metabolic stress with the glycolytic inhibitor iodoacetic acid (1AA, 5 mM) increased tritium release by 63% (P < 0.01), relative to cells treated with buffer alone. The IAA-induced increase was blocked by the nucleoside transport inhibitor nitrobenzylthioinosine (1 microM), indicating that the increased tritium release was primarily a purine nucleoside. HPLC verified this to be [3H]adenosine. The adenosine A1 receptor selective agonist N6-cyclohexyladenosine (CHA, 300 nM) increased the release of [3H]purine nucleoside induced by IAA treatment by 39% (P < 0.05). This increase was blocked by the A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (10 microM). Treatment of cells with UTP (100 microM), histamine (100 microM), or phorbol-12-myristate-13-acetate (PMA, 10 microM) also increased [3H]purine nucleoside release. The protein kinase C inhibitor chelerythrine chloride (500 nM) inhibited the increase in [3H]purine nucleoside efflux induced by CHA or PMA treatment. The adenosine kinase activity of cells treated with CHA or PMA was found to be decreased significantly compared with buffer-treated cells. These data indicated that adenosine A1 receptor activation increased nucleoside efflux from metabolically stressed DDT1 MF-2 cells by a PKC-dependent inhibition of adenosine kinase activity.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">10660114</PMID><DateCreated><Year>2000</Year><Month>03</Month><Day>02</Day></DateCreated><DateCompleted><Year>2000</Year><Month>03</Month><Day>02</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0006-2952</ISSN><JournalIssue CitedMedium="Print"><Volume>59</Volume><Issue>5</Issue><PubDate><Year>2000</Year><Month>Mar</Month><Day>01</Day></PubDate></JournalIssue><Title>Biochemical pharmacology</Title><ISOAbbreviation>Biochem. Pharmacol.</ISOAbbreviation></Journal><ArticleTitle>Stimulation of nucleoside efflux and inhibition of adenosine kinase by A1 adenosine receptor activation.</ArticleTitle><Pagination><MedlinePgn>477-83</MedlinePgn></Pagination><Abstract><AbstractText>Adenosine is produced intracellularly during conditions of metabolic stress and is an endogenous agonist for four subtypes of G-protein linked receptors. Nucleoside transporters are membrane-bound carrier proteins that transfer adenosine, and other nucleosides, across biological membranes. We investigated whether adenosine receptor activation could modulate transporter-mediated adenosine efflux from metabolically stressed cells. DDT1 MF-2 smooth muscle cells were incubated with 10 microM [3H]adenine to label adenine nucleotide pools. Metabolic stress with the glycolytic inhibitor iodoacetic acid (1AA, 5 mM) increased tritium release by 63% (P < 0.01), relative to cells treated with buffer alone. The IAA-induced increase was blocked by the nucleoside transport inhibitor nitrobenzylthioinosine (1 microM), indicating that the increased tritium release was primarily a purine nucleoside. HPLC verified this to be [3H]adenosine. The adenosine A1 receptor selective agonist N6-cyclohexyladenosine (CHA, 300 nM) increased the release of [3H]purine nucleoside induced by IAA treatment by 39% (P < 0.05). This increase was blocked by the A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (10 microM). Treatment of cells with UTP (100 microM), histamine (100 microM), or phorbol-12-myristate-13-acetate (PMA, 10 microM) also increased [3H]purine nucleoside release. The protein kinase C inhibitor chelerythrine chloride (500 nM) inhibited the increase in [3H]purine nucleoside efflux induced by CHA or PMA treatment. The adenosine kinase activity of cells treated with CHA or PMA was found to be decreased significantly compared with buffer-treated cells. These data indicated that adenosine A1 receptor activation increased nucleoside efflux from metabolically stressed DDT1 MF-2 cells by a PKC-dependent inhibition of adenosine kinase activity.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Sinclair</LastName><ForeName>C J</ForeName><Initials>CJ</Initials><AffiliationInfo><Affiliation>Department of Pharmacology and Therapeutics, University of Manitoba, Winnipeg, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shepel</LastName><ForeName>P N</ForeName><Initials>PN</Initials></Author><Author ValidYN="Y"><LastName>Geiger</LastName><ForeName>J D</ForeName><Initials>JD</Initials></Author><Author ValidYN="Y"><LastName>Parkinson</LastName><ForeName>F E</ForeName><Initials>FE</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Biochem Pharmacol</MedlineTA><NlmUniqueID>0101032</NlmUniqueID><ISSNLinking>0006-2952</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D002352">Carrier Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008565">Membrane Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D033703">Nucleoside Transport Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018047">Receptors, Purinergic P1</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.20</RegistryNumber><NameOfSubstance UI="D000248">Adenosine Kinase</NameOfSubstance></Chemical><Chemical><RegistryNumber>K72T3FS567</RegistryNumber><NameOfSubstance UI="D000241">Adenosine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000241" MajorTopicYN="N">Adenosine</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000248" MajorTopicYN="N">Adenosine Kinase</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="Y">antagonists & inhibitors</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001692" MajorTopicYN="N">Biological Transport</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002352" MajorTopicYN="N">Carrier Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006224" MajorTopicYN="N">Cricetinae</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008565" MajorTopicYN="N">Membrane Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D033703" MajorTopicYN="N">Nucleoside Transport Proteins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018047" MajorTopicYN="N">Receptors, Purinergic P1</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014407" MajorTopicYN="N">Tumor Cells, Cultured</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2000</Year><Month>2</Month><Day>5</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2000</Year><Month>3</Month><Day>4</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2000</Year><Month>2</Month><Day>5</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">10660114</ArticleId><ArticleId IdType="pii">S0006-2952(99)00350-0</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Canada</li></country><region><li>Manitoba</li></region><settlement><li>Winnipeg</li></settlement><orgName><li>Université du Manitoba</li></orgName></list><tree><noCountry><name sortKey="Geiger, J D" sort="Geiger, J D" uniqKey="Geiger J" first="J D" last="Geiger">J D Geiger</name><name sortKey="Parkinson, F E" sort="Parkinson, F E" uniqKey="Parkinson F" first="F E" last="Parkinson">F E Parkinson</name><name sortKey="Shepel, P N" sort="Shepel, P N" uniqKey="Shepel P" first="P N" last="Shepel">P N Shepel</name></noCountry><country name="Canada"><region name="Manitoba"><name sortKey="Sinclair, C J" sort="Sinclair, C J" uniqKey="Sinclair C" first="C J" last="Sinclair">C J Sinclair</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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