Nitric oxide reduces adenosine transporter ENT1 gene (SLC29A1) promoter activity in human fetal endothelium from gestational diabetes
Identifieur interne : 002E12 ( Main/Exploration ); précédent : 002E11; suivant : 002E13Nitric oxide reduces adenosine transporter ENT1 gene (SLC29A1) promoter activity in human fetal endothelium from gestational diabetes
Auteurs : Marcelo Farías [Chili] ; Rody San Martín [Chili] ; Carlos Puebla [Chili] ; Jeremy D. Pearson [Royaume-Uni] ; Javier F. Casado [Espagne] ; Marçal Pastor-Anglada [Espagne] ; Paola Casanello [Chili] ; Luis Sobrevia [Chili]Source :
- Journal of Cellular Physiology [ 0021-9541 ] ; 2006-08.
English descriptors
- Teeft :
- Actinomycin, Adenosine, Adenosine transport, Adenosine uptake, Aguayo, Casanello, Cell type, Cell types, Cellular physiology, Chile, Densitometry, Diabetes, Diabetic, Diabetic cells, Diabetic cells transfected, Endothelium, Enos, Equilibrative, Fetal, Gestational, Gestational diabetes, Gestational diabetes exhibit, Hent1, Hent1 expression, Hent1 mrna level, Hent1 protein abundance, Human umbilical vein, Human umbilical vein endothelium, Huvec, Lname, Luciferase, Methyl ester, Mrna, Mrna level, Mrna ratio densitometry, Nbmpr, Ndings, Nitric, Nitric oxide, Normal cells, Normal pregnancies, Nucleoside, Other values, Overall adenosine transport, Physiol, Primary cultures, Promega, Promoter, Promoter activity, Protein ratio densitometry, Reporter activity, Results show, Right part, Similar values, Sirna, Sobrevia, Transcription, Transcriptional, Transfected, Transporter, Umbilical, Umbilical vein, Unaltered, Vasquez, Vmax, Western blot.
Abstract
Human umbilical vein endothelial cells (HUVEC) from gestational diabetes exhibit reduced adenosine uptake and increased nitric oxide (NO) synthesis. Adenosine transport via human equilibrative nucleoside transporters 1 (hENT1) is reduced by NO by unknown mechanisms in HUVEC. We examined whether gestational diabetes‐reduced adenosine transport results from lower hENT1 gene (SLC29A1) expression. HUVEC from gestational diabetes exhibit reduced SLC29A1 promoter activity when transfected with pGL3‐hENT1−2154 compared with pGL3‐hENT1−1114 constructs, an effect blocked by NG‐nitro‐L‐arginine methyl ester (L‐NAME, NOS inhibitor), but unaltered by S‐nitroso‐N‐acetyl‐L,D‐penicillamine (SNAP, NO donor). In cells from gestational diabetes transfected with pGL3‐hENT1−2154, L‐NAME increased, but SNAP did not alter promoter activity and hENT1 expression. However, in cells from normal pregnancies L‐NAME increased, but SNAP reduced promoter activity and hENT1 expression. Adenovirus‐silenced eNOS expression increased hENT1 expression and activity in cells from normal or gestational diabetic pregnancies. Thus, reduced adenosine transport may result from downregulation of SLC29A1 expression by NO in HUVEC from gestational diabetes. These findings explain the accumulation of extracellular adenosine detected in cultures of HUVEC from gestational diabetes. In addition, fetal endothelial dysfunction could be involved in the abnormal fetal development and growth seen in gestational diabetes. J. Cell. Physiol. 208: 451–460, 2006. © 2006 Wiley‐Liss, Inc.
Url:
DOI: 10.1002/jcp.20680
Affiliations:
- Chili, Espagne, Royaume-Uni
- Angleterre, Catalogne, Grand Londres
- Barcelone, Londres
- Université de Barcelone
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Pearson</name><affiliation wicri:level="3"><country>Royaume-Uni</country><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName><wicri:orgArea>Biomedical Sciences Division, King's College London, University of London</wicri:orgArea></affiliation></author><author><name sortKey="Casado, Javier F" sort="Casado, Javier F" uniqKey="Casado J" first="Javier F." last="Casado">Javier F. Casado</name><affiliation wicri:level="4"><country xml:lang="fr">Espagne</country><wicri:regionArea>Departament de Bioquímica i Biologia Molecular, Universitat de Barcelona, Barcelona</wicri:regionArea><placeName><settlement type="city">Barcelone</settlement><region nuts="2" type="region">Catalogne</region></placeName><orgName type="university">Université de Barcelone</orgName></affiliation></author><author><name sortKey="Pastor Nglada, Marcal" sort="Pastor Nglada, Marcal" uniqKey="Pastor Nglada M" first="Marçal" last="Pastor-Anglada">Marçal Pastor-Anglada</name><affiliation wicri:level="4"><country xml:lang="fr">Espagne</country><wicri:regionArea>Departament de Bioquímica i Biologia Molecular, Universitat de Barcelona, Barcelona</wicri:regionArea><placeName><settlement type="city">Barcelone</settlement><region nuts="2" type="region">Catalogne</region></placeName><orgName type="university">Université de Barcelone</orgName></affiliation></author><author><name sortKey="Casanello, Paola" sort="Casanello, Paola" uniqKey="Casanello P" first="Paola" last="Casanello">Paola Casanello</name><affiliation wicri:level="1"><country xml:lang="fr">Chili</country><wicri:regionArea>Cellular and Molecular Physiology Laboratory (CMPL), Department of Obstetrics and Gynaecology, Medical Research Centre (CIM), School of Medicine, Faculty of Medicine, Pontificia Universidad Católica de Chile, Santiago</wicri:regionArea><wicri:noRegion>Santiago</wicri:noRegion></affiliation></author><author><name sortKey="Sobrevia, Luis" sort="Sobrevia, Luis" uniqKey="Sobrevia L" first="Luis" last="Sobrevia">Luis Sobrevia</name><affiliation wicri:level="1"><country xml:lang="fr">Chili</country><wicri:regionArea>Cellular and Molecular Physiology Laboratory (CMPL), Department of Obstetrics and Gynaecology, Medical Research Centre (CIM), School of Medicine, Faculty of Medicine, Pontificia Universidad Católica de Chile, Santiago</wicri:regionArea><wicri:noRegion>Santiago</wicri:noRegion></affiliation><affiliation wicri:level="1"><country wicri:rule="url">Chili</country></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Chili</country><wicri:regionArea>Correspondence address: Cellular and Molecular Physiology Laboratory (CMPL), Medical Research Centre (CIM), Department of Obstetrics and Gynaecology, School of Medicine, Faculty of Medicine, Pontificia Universidad Católica de Chile, P.O. Box 114‐D, Santiago</wicri:regionArea><wicri:noRegion>Santiago</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Journal of Cellular Physiology</title><title level="j" type="alt">JOURNAL OF CELLULAR PHYSIOLOGY</title><idno type="ISSN">0021-9541</idno><idno type="eISSN">1097-4652</idno><imprint><biblScope unit="vol">208</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="451">451</biblScope><biblScope unit="page" to="460">460</biblScope><biblScope unit="page-count">10</biblScope><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2006-08">2006-08</date></imprint><idno type="ISSN">0021-9541</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0021-9541</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Actinomycin</term><term>Adenosine</term><term>Adenosine transport</term><term>Adenosine uptake</term><term>Aguayo</term><term>Casanello</term><term>Cell type</term><term>Cell types</term><term>Cellular physiology</term><term>Chile</term><term>Densitometry</term><term>Diabetes</term><term>Diabetic</term><term>Diabetic cells</term><term>Diabetic cells transfected</term><term>Endothelium</term><term>Enos</term><term>Equilibrative</term><term>Fetal</term><term>Gestational</term><term>Gestational diabetes</term><term>Gestational diabetes exhibit</term><term>Hent1</term><term>Hent1 expression</term><term>Hent1 mrna level</term><term>Hent1 protein abundance</term><term>Human umbilical vein</term><term>Human umbilical vein endothelium</term><term>Huvec</term><term>Lname</term><term>Luciferase</term><term>Methyl ester</term><term>Mrna</term><term>Mrna level</term><term>Mrna ratio densitometry</term><term>Nbmpr</term><term>Ndings</term><term>Nitric</term><term>Nitric oxide</term><term>Normal cells</term><term>Normal pregnancies</term><term>Nucleoside</term><term>Other values</term><term>Overall adenosine transport</term><term>Physiol</term><term>Primary cultures</term><term>Promega</term><term>Promoter</term><term>Promoter activity</term><term>Protein ratio densitometry</term><term>Reporter activity</term><term>Results show</term><term>Right part</term><term>Similar values</term><term>Sirna</term><term>Sobrevia</term><term>Transcription</term><term>Transcriptional</term><term>Transfected</term><term>Transporter</term><term>Umbilical</term><term>Umbilical vein</term><term>Unaltered</term><term>Vasquez</term><term>Vmax</term><term>Western blot</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Human umbilical vein endothelial cells (HUVEC) from gestational diabetes exhibit reduced adenosine uptake and increased nitric oxide (NO) synthesis. Adenosine transport via human equilibrative nucleoside transporters 1 (hENT1) is reduced by NO by unknown mechanisms in HUVEC. We examined whether gestational diabetes‐reduced adenosine transport results from lower hENT1 gene (SLC29A1) expression. HUVEC from gestational diabetes exhibit reduced SLC29A1 promoter activity when transfected with pGL3‐hENT1−2154 compared with pGL3‐hENT1−1114 constructs, an effect blocked by NG‐nitro‐L‐arginine methyl ester (L‐NAME, NOS inhibitor), but unaltered by S‐nitroso‐N‐acetyl‐L,D‐penicillamine (SNAP, NO donor). In cells from gestational diabetes transfected with pGL3‐hENT1−2154, L‐NAME increased, but SNAP did not alter promoter activity and hENT1 expression. However, in cells from normal pregnancies L‐NAME increased, but SNAP reduced promoter activity and hENT1 expression. Adenovirus‐silenced eNOS expression increased hENT1 expression and activity in cells from normal or gestational diabetic pregnancies. Thus, reduced adenosine transport may result from downregulation of SLC29A1 expression by NO in HUVEC from gestational diabetes. These findings explain the accumulation of extracellular adenosine detected in cultures of HUVEC from gestational diabetes. In addition, fetal endothelial dysfunction could be involved in the abnormal fetal development and growth seen in gestational diabetes. J. Cell. Physiol. 208: 451–460, 2006. © 2006 Wiley‐Liss, Inc.</div></front></TEI><affiliations><list><country><li>Chili</li><li>Espagne</li><li>Royaume-Uni</li></country><region><li>Angleterre</li><li>Catalogne</li><li>Grand Londres</li></region><settlement><li>Barcelone</li><li>Londres</li></settlement><orgName><li>Université de Barcelone</li></orgName></list><tree><country name="Chili"><noRegion><name sortKey="Farias, Marcelo" sort="Farias, Marcelo" uniqKey="Farias M" first="Marcelo" last="Farías">Marcelo Farías</name></noRegion><name sortKey="Casanello, Paola" sort="Casanello, Paola" uniqKey="Casanello P" first="Paola" last="Casanello">Paola Casanello</name><name sortKey="Puebla, Carlos" sort="Puebla, Carlos" uniqKey="Puebla C" first="Carlos" last="Puebla">Carlos Puebla</name><name sortKey="San Martin, Rody" sort="San Martin, Rody" uniqKey="San Martin R" first="Rody" last="San Martín">Rody San Martín</name><name sortKey="Sobrevia, Luis" sort="Sobrevia, Luis" uniqKey="Sobrevia L" first="Luis" last="Sobrevia">Luis Sobrevia</name><name sortKey="Sobrevia, Luis" sort="Sobrevia, Luis" uniqKey="Sobrevia L" first="Luis" last="Sobrevia">Luis Sobrevia</name><name sortKey="Sobrevia, Luis" sort="Sobrevia, Luis" uniqKey="Sobrevia L" first="Luis" last="Sobrevia">Luis Sobrevia</name></country><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Pearson, Jeremy D" sort="Pearson, Jeremy D" uniqKey="Pearson J" first="Jeremy D." last="Pearson">Jeremy D. Pearson</name></region></country><country name="Espagne"><region name="Catalogne"><name sortKey="Casado, Javier F" sort="Casado, Javier F" uniqKey="Casado J" first="Javier F." last="Casado">Javier F. Casado</name></region><name sortKey="Pastor Nglada, Marcal" sort="Pastor Nglada, Marcal" uniqKey="Pastor Nglada M" first="Marçal" last="Pastor-Anglada">Marçal Pastor-Anglada</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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