Gene expression for enzymes and transporters involved in regulating adenosine and inosine levels in rat forebrain neurons, astrocytes and C6 glioma cells
Identifieur interne : 002838 ( Main/Exploration ); précédent : 002837; suivant : 002839Gene expression for enzymes and transporters involved in regulating adenosine and inosine levels in rat forebrain neurons, astrocytes and C6 glioma cells
Auteurs : Fiona E. Parkinson [Canada] ; Jennifer Ferguson [Canada] ; Christina R. Zamzow [Canada] ; Wei Xiong [Canada]Source :
- Journal of Neuroscience Research [ 0360-4012 ] ; 2006-09.
English descriptors
- KwdEn :
- AMP deaminase, Adenosine (metabolism), Animals, Astrocytes (metabolism), Cells, Cultured, Cloning, Molecular (methods), Enzymes (genetics), Enzymes (metabolism), Gene Expression (physiology), Glioma (metabolism), Inosine (metabolism), Mice, Neurons (metabolism), Nucleotide Transport Proteins (genetics), Nucleotide Transport Proteins (metabolism), Prosencephalon (cytology), RNA, Messenger (metabolism), Rats, Reverse Transcriptase Polymerase Chain Reaction (methods), Tritium (metabolism), brain, cytosolic nucleotidases, ecto 5′nucleotidase, nucleoside transport, purines.
- MESH :
- chemical , genetics : Enzymes, Nucleotide Transport Proteins.
- chemical , metabolism : Adenosine, Enzymes, Inosine, Nucleotide Transport Proteins, RNA, Messenger, Tritium.
- cytology : Prosencephalon.
- metabolism : Astrocytes, Glioma, Neurons.
- methods : Cloning, Molecular, Reverse Transcriptase Polymerase Chain Reaction.
- physiology : Gene Expression.
- Animals, Cells, Cultured, Mice, Rats.
Abstract
In brain, levels of adenosine increase up to 100‐fold during cerebral ischemia. Based on in vitro studies, both astrocytes and neurons contribute to this adenosine release. Neurons release adenosine per se whereas astrocytes release adenine nucleotides that are metabolized to adenosine extracellularly. In contrast, inosine is released from both cell types via a nucleoside transporter. C6 glioma cells, which are derived from astrocytes, release inosine but not adenosine. The present study investigated the relative expression of purine metabolizing enzymes and transporters in neurons, astrocytes and C6 glioma cells by real‐time PCR analysis. In agreement with the extracellular formation of adenosine and intracellular formation of inosine by astrocytes, the present study showed high expression of ecto 5′‐nucleotidase and AMP deaminase type 3 in astrocytes. The lack of adenosine release from C6 glioma cells was consistent with the absence of expression of the AMP‐preferring cytosolic 5′‐nucleotidase in these cells. The predominance of nitrobenzylthioinosine (NBMPR) insensitive equilibrative nucleoside transport (ENT2) in all three cell types was consistent with the greater activity of this isoform in comparison to NBMPR‐sensitive ENT1 in these rat cells. Thus, cell type differences in adenosine formation and release are primarily a function of differences in expression of purinergic enzymes and transporters. © 2006 Wiley‐Liss, Inc.
Url:
DOI: 10.1002/jnr.20988
Affiliations:
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Parkinson</name><affiliation wicri:level="4"><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><affiliation></affiliation></author><author><name sortKey="Ferguson, Jennifer" sort="Ferguson, Jennifer" uniqKey="Ferguson J" first="Jennifer" last="Ferguson">Jennifer Ferguson</name><affiliation wicri:level="4"><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="Zamzow, Christina R" sort="Zamzow, Christina R" uniqKey="Zamzow C" first="Christina R." last="Zamzow">Christina R. Zamzow</name><affiliation wicri:level="4"><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="Xiong, Wei" sort="Xiong, Wei" uniqKey="Xiong W" first="Wei" last="Xiong">Wei Xiong</name><affiliation wicri:level="4"><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></analytic><monogr></monogr><series><title level="j">Journal of Neuroscience Research</title><title level="j" type="abbrev">J. Neurosci. Res.</title><idno type="ISSN">0360-4012</idno><idno type="eISSN">1097-4547</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2006-09">2006-09</date><biblScope unit="volume">84</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="801">801</biblScope><biblScope unit="page" to="808">808</biblScope></imprint><idno type="ISSN">0360-4012</idno></series><idno type="istex">9057F88B2B98ABA163BEFDD643AEC7986D88B791</idno><idno type="DOI">10.1002/jnr.20988</idno><idno type="ArticleID">JNR20988</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0360-4012</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>AMP deaminase</term><term>Adenosine (metabolism)</term><term>Animals</term><term>Astrocytes (metabolism)</term><term>Cells, Cultured</term><term>Cloning, Molecular (methods)</term><term>Enzymes (genetics)</term><term>Enzymes (metabolism)</term><term>Gene Expression (physiology)</term><term>Glioma (metabolism)</term><term>Inosine (metabolism)</term><term>Mice</term><term>Neurons (metabolism)</term><term>Nucleotide Transport Proteins (genetics)</term><term>Nucleotide Transport Proteins (metabolism)</term><term>Prosencephalon (cytology)</term><term>RNA, Messenger (metabolism)</term><term>Rats</term><term>Reverse Transcriptase Polymerase Chain Reaction (methods)</term><term>Tritium (metabolism)</term><term>brain</term><term>cytosolic nucleotidases</term><term>ecto 5′nucleotidase</term><term>nucleoside transport</term><term>purines</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Enzymes</term><term>Nucleotide Transport Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Adenosine</term><term>Enzymes</term><term>Inosine</term><term>Nucleotide Transport Proteins</term><term>RNA, Messenger</term><term>Tritium</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Prosencephalon</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Astrocytes</term><term>Glioma</term><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Cloning, Molecular</term><term>Reverse Transcriptase Polymerase Chain Reaction</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Gene Expression</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cells, Cultured</term><term>Mice</term><term>Rats</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In brain, levels of adenosine increase up to 100‐fold during cerebral ischemia. Based on in vitro studies, both astrocytes and neurons contribute to this adenosine release. Neurons release adenosine per se whereas astrocytes release adenine nucleotides that are metabolized to adenosine extracellularly. In contrast, inosine is released from both cell types via a nucleoside transporter. C6 glioma cells, which are derived from astrocytes, release inosine but not adenosine. The present study investigated the relative expression of purine metabolizing enzymes and transporters in neurons, astrocytes and C6 glioma cells by real‐time PCR analysis. In agreement with the extracellular formation of adenosine and intracellular formation of inosine by astrocytes, the present study showed high expression of ecto 5′‐nucleotidase and AMP deaminase type 3 in astrocytes. The lack of adenosine release from C6 glioma cells was consistent with the absence of expression of the AMP‐preferring cytosolic 5′‐nucleotidase in these cells. The predominance of nitrobenzylthioinosine (NBMPR) insensitive equilibrative nucleoside transport (ENT2) in all three cell types was consistent with the greater activity of this isoform in comparison to NBMPR‐sensitive ENT1 in these rat cells. Thus, cell type differences in adenosine formation and release are primarily a function of differences in expression of purinergic enzymes and transporters. © 2006 Wiley‐Liss, Inc.</div></front></TEI><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><country name="Canada"><region name="Manitoba"><name sortKey="Parkinson, Fiona E" sort="Parkinson, Fiona E" uniqKey="Parkinson F" first="Fiona E." last="Parkinson">Fiona E. Parkinson</name></region><name sortKey="Ferguson, Jennifer" sort="Ferguson, Jennifer" uniqKey="Ferguson J" first="Jennifer" last="Ferguson">Jennifer Ferguson</name><name sortKey="Xiong, Wei" sort="Xiong, Wei" uniqKey="Xiong W" first="Wei" last="Xiong">Wei Xiong</name><name sortKey="Zamzow, Christina R" sort="Zamzow, Christina R" uniqKey="Zamzow C" first="Christina R." last="Zamzow">Christina R. Zamzow</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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