Effect of ecto-5'-nucleotidase (eN) in astrocytes on adenosine and inosine formation.
Identifieur interne : 000635 ( PubMed/Curation ); précédent : 000634; suivant : 000636Effect of ecto-5'-nucleotidase (eN) in astrocytes on adenosine and inosine formation.
Auteurs : Stephanie Chu [Canada] ; Wei Xiong ; Fiona E. ParkinsonSource :
- Purinergic signalling [ 1573-9546 ] ; 2014.
English descriptors
- KwdEn :
- MESH :
- chemical , biosynthesis : Adenosine, Inosine.
- chemical , metabolism : 5'-Nucleotidase.
- metabolism : Astrocytes, Ischemia, Neurons.
- physiology : Cell Hypoxia.
- Animals, Cells, Cultured, Coculture Techniques, Mice, Mice, Knockout.
Abstract
ATP is a gliotransmitter released from astrocytes. Extracellularly, ATP is metabolized by a series of enzymes, including ecto-5'-nucleotidase (eN; also known as CD73) which is encoded by the gene 5NTE and functions to form adenosine (ADO) from adenosine monophosphate (AMP). Under ischemic conditions, ADO levels in brain increase up to 100-fold. We used astrocytes cultured from 5NTE (+/+) or 5NTE (-/-) mice to evaluate the role of eN expressed by astrocytes in the production of ADO and inosine (INO) in response to glucose deprivation (GD) or oxygen-glucose deprivation (OGD). We also used co-cultures of these astrocytes with wild-type neurons to evaluate the role of eN expressed by astrocytes in the production of ADO and INO in response to GD, OGD, or N-methyl-D-aspartate (NMDA) treatment. As expected, astrocytes from 5NTE (+/+) mice produced adenosine from AMP; the eN inhibitor α,β-methylene ADP (AOPCP) decreased ADO formation. In contrast, little ADO was formed by astrocytes from 5NTE (-/-) mice and AOPCP had no significant effect. GD and OGD treatment of 5NTE (+/+) astrocytes and 5NTE (+/+) astrocyte-neuron co-cultures produced extracellular ADO levels that were inhibited by AOPCP. In contrast, these conditions did not evoke ADO production in cultures containing 5NTE (-/-) astrocytes. NMDA treatment produced similar increases in ADO in both 5NTE (+/+) and 5NTE (-/-) astrocyte-neuron co-cultures; dipyridamole (DPR) but not AOPCP inhibited ADO production. These results indicate that eN is prominent in the formation of ADO from astrocytes but in astrocyte-neuron co-cultures, other enzymes or pathways contribute to rising ADO levels in ischemia-like conditions.
DOI: 10.1007/s11302-014-9421-8
PubMed: 25129451
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Effect of ecto-5'-nucleotidase (eN) in astrocytes on adenosine and inosine formation.</title><author><name sortKey="Chu, Stephanie" sort="Chu, Stephanie" uniqKey="Chu S" first="Stephanie" last="Chu">Stephanie Chu</name><affiliation wicri:level="1"><nlm:affiliation>Department of Pharmacology and Therapeutics, University of Manitoba, A203-753 McDermot Avenue, Winnipeg, MB, R3E 0T6, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Pharmacology and Therapeutics, University of Manitoba, A203-753 McDermot Avenue, Winnipeg, MB, R3E 0T6</wicri:regionArea></affiliation></author><author><name sortKey="Xiong, Wei" sort="Xiong, Wei" uniqKey="Xiong W" first="Wei" last="Xiong">Wei Xiong</name></author><author><name sortKey="Parkinson, Fiona E" sort="Parkinson, Fiona E" uniqKey="Parkinson F" first="Fiona E" last="Parkinson">Fiona E. Parkinson</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2014">2014</date><idno type="RBID">pubmed:25129451</idno><idno type="pmid">25129451</idno><idno type="doi">10.1007/s11302-014-9421-8</idno><idno type="wicri:Area/PubMed/Corpus">000635</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000635</idno><idno type="wicri:Area/PubMed/Curation">000635</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000635</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Effect of ecto-5'-nucleotidase (eN) in astrocytes on adenosine and inosine formation.</title><author><name sortKey="Chu, Stephanie" sort="Chu, Stephanie" uniqKey="Chu S" first="Stephanie" last="Chu">Stephanie Chu</name><affiliation wicri:level="1"><nlm:affiliation>Department of Pharmacology and Therapeutics, University of Manitoba, A203-753 McDermot Avenue, Winnipeg, MB, R3E 0T6, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Pharmacology and Therapeutics, University of Manitoba, A203-753 McDermot Avenue, Winnipeg, MB, R3E 0T6</wicri:regionArea></affiliation></author><author><name sortKey="Xiong, Wei" sort="Xiong, Wei" uniqKey="Xiong W" first="Wei" last="Xiong">Wei Xiong</name></author><author><name sortKey="Parkinson, Fiona E" sort="Parkinson, Fiona E" uniqKey="Parkinson F" first="Fiona E" last="Parkinson">Fiona E. Parkinson</name></author></analytic><series><title level="j">Purinergic signalling</title><idno type="eISSN">1573-9546</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>5'-Nucleotidase (metabolism)</term><term>Adenosine (biosynthesis)</term><term>Animals</term><term>Astrocytes (metabolism)</term><term>Cell Hypoxia (physiology)</term><term>Cells, Cultured</term><term>Coculture Techniques</term><term>Inosine (biosynthesis)</term><term>Ischemia (metabolism)</term><term>Mice</term><term>Mice, Knockout</term><term>Neurons (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Adenosine</term><term>Inosine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>5'-Nucleotidase</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Astrocytes</term><term>Ischemia</term><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Cell Hypoxia</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cells, Cultured</term><term>Coculture Techniques</term><term>Mice</term><term>Mice, Knockout</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">ATP is a gliotransmitter released from astrocytes. Extracellularly, ATP is metabolized by a series of enzymes, including ecto-5'-nucleotidase (eN; also known as CD73) which is encoded by the gene 5NTE and functions to form adenosine (ADO) from adenosine monophosphate (AMP). Under ischemic conditions, ADO levels in brain increase up to 100-fold. We used astrocytes cultured from 5NTE (+/+) or 5NTE (-/-) mice to evaluate the role of eN expressed by astrocytes in the production of ADO and inosine (INO) in response to glucose deprivation (GD) or oxygen-glucose deprivation (OGD). We also used co-cultures of these astrocytes with wild-type neurons to evaluate the role of eN expressed by astrocytes in the production of ADO and INO in response to GD, OGD, or N-methyl-D-aspartate (NMDA) treatment. As expected, astrocytes from 5NTE (+/+) mice produced adenosine from AMP; the eN inhibitor α,β-methylene ADP (AOPCP) decreased ADO formation. In contrast, little ADO was formed by astrocytes from 5NTE (-/-) mice and AOPCP had no significant effect. GD and OGD treatment of 5NTE (+/+) astrocytes and 5NTE (+/+) astrocyte-neuron co-cultures produced extracellular ADO levels that were inhibited by AOPCP. In contrast, these conditions did not evoke ADO production in cultures containing 5NTE (-/-) astrocytes. NMDA treatment produced similar increases in ADO in both 5NTE (+/+) and 5NTE (-/-) astrocyte-neuron co-cultures; dipyridamole (DPR) but not AOPCP inhibited ADO production. These results indicate that eN is prominent in the formation of ADO from astrocytes but in astrocyte-neuron co-cultures, other enzymes or pathways contribute to rising ADO levels in ischemia-like conditions.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25129451</PMID><DateCreated><Year>2014</Year><Month>12</Month><Day>20</Day></DateCreated><DateCompleted><Year>2015</Year><Month>12</Month><Day>29</Day></DateCompleted><DateRevised><Year>2016</Year><Month>10</Month><Day>19</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1573-9546</ISSN><JournalIssue CitedMedium="Internet"><Volume>10</Volume><Issue>4</Issue><PubDate><Year>2014</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Purinergic signalling</Title><ISOAbbreviation>Purinergic Signal.</ISOAbbreviation></Journal><ArticleTitle>Effect of ecto-5'-nucleotidase (eN) in astrocytes on adenosine and inosine formation.</ArticleTitle><Pagination><MedlinePgn>603-9</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s11302-014-9421-8</ELocationID><Abstract><AbstractText>ATP is a gliotransmitter released from astrocytes. Extracellularly, ATP is metabolized by a series of enzymes, including ecto-5'-nucleotidase (eN; also known as CD73) which is encoded by the gene 5NTE and functions to form adenosine (ADO) from adenosine monophosphate (AMP). Under ischemic conditions, ADO levels in brain increase up to 100-fold. We used astrocytes cultured from 5NTE (+/+) or 5NTE (-/-) mice to evaluate the role of eN expressed by astrocytes in the production of ADO and inosine (INO) in response to glucose deprivation (GD) or oxygen-glucose deprivation (OGD). We also used co-cultures of these astrocytes with wild-type neurons to evaluate the role of eN expressed by astrocytes in the production of ADO and INO in response to GD, OGD, or N-methyl-D-aspartate (NMDA) treatment. As expected, astrocytes from 5NTE (+/+) mice produced adenosine from AMP; the eN inhibitor α,β-methylene ADP (AOPCP) decreased ADO formation. In contrast, little ADO was formed by astrocytes from 5NTE (-/-) mice and AOPCP had no significant effect. GD and OGD treatment of 5NTE (+/+) astrocytes and 5NTE (+/+) astrocyte-neuron co-cultures produced extracellular ADO levels that were inhibited by AOPCP. In contrast, these conditions did not evoke ADO production in cultures containing 5NTE (-/-) astrocytes. NMDA treatment produced similar increases in ADO in both 5NTE (+/+) and 5NTE (-/-) astrocyte-neuron co-cultures; dipyridamole (DPR) but not AOPCP inhibited ADO production. These results indicate that eN is prominent in the formation of ADO from astrocytes but in astrocyte-neuron co-cultures, other enzymes or pathways contribute to rising ADO levels in ischemia-like conditions.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Chu</LastName><ForeName>Stephanie</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Pharmacology and Therapeutics, University of Manitoba, A203-753 McDermot Avenue, Winnipeg, MB, R3E 0T6, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xiong</LastName><ForeName>Wei</ForeName><Initials>W</Initials></Author><Author ValidYN="Y"><LastName>Parkinson</LastName><ForeName>Fiona E</ForeName><Initials>FE</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><Agency>Canadian Institutes of Health Research</Agency><Country>Canada</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>08</Month><Day>17</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Purinergic Signal</MedlineTA><NlmUniqueID>101250499</NlmUniqueID><ISSNLinking>1573-9538</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>5A614L51CT</RegistryNumber><NameOfSubstance UI="D007288">Inosine</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.1.3.5</RegistryNumber><NameOfSubstance UI="D015720">5'-Nucleotidase</NameOfSubstance></Chemical><Chemical><RegistryNumber>K72T3FS567</RegistryNumber><NameOfSubstance UI="D000241">Adenosine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>PLoS One. 2012;7(6):e39772</RefSource><PMID 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UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading></MeshHeadingList><OtherID Source="NLM">PMC4272361</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2014</Year><Month>05</Month><Day>07</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2014</Year><Month>07</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2014</Year><Month>8</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2014</Year><Month>8</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2015</Year><Month>12</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">25129451</ArticleId><ArticleId IdType="doi">10.1007/s11302-014-9421-8</ArticleId><ArticleId 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