Nitric oxide reduces adenosine transporter ENT1 gene (SLC29A1) promoter activity in human fetal endothelium from gestational diabetes
Identifieur interne : 001B71 ( Istex/Corpus ); précédent : 001B70; suivant : 001B72Nitric oxide reduces adenosine transporter ENT1 gene (SLC29A1) promoter activity in human fetal endothelium from gestational diabetes
Auteurs : Marcelo Farías ; Rody San Martín ; Carlos Puebla ; Jeremy D. Pearson ; Javier F. Casado ; Marçal Pastor-Anglada ; Paola Casanello ; Luis SobreviaSource :
- 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
Links to Exploration step
ISTEX:9187712C25082F809449CE9A8F0BC79130B5A415Le document en format XML
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Box 114‐D, Santiago, Chile.</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:9187712C25082F809449CE9A8F0BC79130B5A415</idno><date when="2006" year="2006">2006</date><idno type="doi">10.1002/jcp.20680</idno><idno type="url">https://api.istex.fr/ark:/67375/WNG-C399R479-V/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">001B71</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">001B71</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main">Nitric oxide reduces adenosine transporter ENT1 gene (SLC29A1) promoter activity in human fetal endothelium from gestational diabetes</title><author><name sortKey="Farias, Marcelo" sort="Farias, Marcelo" uniqKey="Farias M" first="Marcelo" last="Farías">Marcelo Farías</name><affiliation><mods:affiliation>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, Chile</mods:affiliation></affiliation></author><author><name sortKey="San Martin, Rody" sort="San Martin, Rody" uniqKey="San Martin R" first="Rody" last="San Martín">Rody San Martín</name><affiliation><mods:affiliation>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, Chile</mods:affiliation></affiliation></author><author><name sortKey="Puebla, Carlos" sort="Puebla, Carlos" uniqKey="Puebla C" first="Carlos" last="Puebla">Carlos Puebla</name><affiliation><mods:affiliation>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, Chile</mods:affiliation></affiliation></author><author><name sortKey="Pearson, Jeremy D" sort="Pearson, Jeremy D" uniqKey="Pearson J" first="Jeremy D." last="Pearson">Jeremy D. Pearson</name><affiliation><mods:affiliation>Biomedical Sciences Division, King's College London, University of London, London</mods:affiliation></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><mods:affiliation>Departament de Bioquímica i Biologia Molecular, Universitat de Barcelona, Barcelona, Spain</mods:affiliation></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><mods:affiliation>Departament de Bioquímica i Biologia Molecular, Universitat de Barcelona, Barcelona, Spain</mods:affiliation></affiliation></author><author><name sortKey="Casanello, Paola" sort="Casanello, Paola" uniqKey="Casanello P" first="Paola" last="Casanello">Paola Casanello</name><affiliation><mods:affiliation>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, Chile</mods:affiliation></affiliation></author><author><name sortKey="Sobrevia, Luis" sort="Sobrevia, Luis" uniqKey="Sobrevia L" first="Luis" last="Sobrevia">Luis Sobrevia</name><affiliation><mods:affiliation>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, Chile</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: sobrevia@med.puc.cl</mods:affiliation></affiliation><affiliation><mods:affiliation>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, Chile.</mods:affiliation></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. 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Pearson</name><affiliations><json:string>Biomedical Sciences Division, King's College London, University of London, London</json:string></affiliations></json:item><json:item><name>Javier F. Casado</name><affiliations><json:string>Departament de Bioquímica i Biologia Molecular, Universitat de Barcelona, Barcelona, Spain</json:string></affiliations></json:item><json:item><name>Marçal Pastor‐Anglada</name><affiliations><json:string>Departament de Bioquímica i Biologia Molecular, Universitat de Barcelona, Barcelona, Spain</json:string></affiliations></json:item><json:item><name>Paola Casanello</name><affiliations><json:string>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, Chile</json:string></affiliations></json:item><json:item><name>Luis Sobrevia</name><affiliations><json:string>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, Chile</json:string><json:string>E-mail: sobrevia@med.puc.cl</json:string><json:string>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, Chile.</json:string></affiliations></json:item></author><articleId><json:string>JCP20680</json:string></articleId><arkIstex>ark:/67375/WNG-C399R479-V</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><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.</abstract><qualityIndicators><score>9.4</score><pdfWordCount>6685</pdfWordCount><pdfCharCount>44005</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>10</pdfPageCount><pdfPageSize>592 x 789 pts</pdfPageSize><pdfWordsPerPage>669</pdfWordsPerPage><pdfText>true</pdfText><refBibsNative>true</refBibsNative><abstractWordCount>200</abstractWordCount><abstractCharCount>1553</abstractCharCount><keywordCount>0</keywordCount></qualityIndicators><title>Nitric oxide reduces adenosine transporter ENT1 gene (SLC29A1) promoter activity in human fetal endothelium from gestational diabetes</title><pmid><json:string>16688763</json:string></pmid><genre><json:string>article</json:string></genre><host><title>Journal of Cellular Physiology</title><language><json:string>unknown</json:string></language><doi><json:string>10.1002/(ISSN)1097-4652</json:string></doi><issn><json:string>0021-9541</json:string></issn><eissn><json:string>1097-4652</json:string></eissn><publisherId><json:string>JCP</json:string></publisherId><volume>208</volume><issue>2</issue><pages><first>451</first><last>460</last><total>10</total></pages><genre><json:string>journal</json:string></genre><subject><json:item><value>Original Article</value></json:item><json:item><value>Original Articles</value></json:item></subject></host><namedEntities><unitex><date><json:string>2006</json:string><json:string>28S</json:string></date><geogName><json:string>San</json:string><json:string>Sawa</json:string></geogName><orgName><json:string>Chile Ethics Committee</json:string><json:string>Medical Research Centre</json:string><json:string>Clontech, Palo Alto</json:string><json:string>Chile, Medicine, Faculty of Medicine, Ponti</json:string><json:string>Department of Obstetrics and Gynaecology</json:string><json:string>Spain Human</json:string><json:string>BioRad Laboratories</json:string><json:string>CIM</json:string><json:string>GIBCO Invitrogen Corporation</json:string><json:string>Hospital Cl</json:string><json:string>Santa Cruz Biotechnology</json:string><json:string>Calbiochem</json:string><json:string>Hospital Luis Tisne Brousse</json:string><json:string>Wiley-Liss, Inc</json:string><json:string>GIBCO Life Technologies</json:string><json:string>University of London</json:string><json:string>LISS, INC.</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Luis Sobrevia</json:string><json:string>P.O. 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EXPRESSION</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><licence>Copyright © 2006 Wiley‐Liss, Inc.</licence></availability><date type="published" when="2006-08"></date></publicationStmt><notesStmt><note type="content-type" subtype="article" source="article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</note><note type="publication-type" subtype="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note></notesStmt><sourceDesc><biblStruct type="article"><analytic><title level="a" type="main">Nitric oxide reduces adenosine transporter ENT1 gene (SLC29A1) promoter activity in human fetal endothelium from gestational diabetes</title><title level="a" type="short" xml:lang="en">NITRIC OXIDE‐REDUCED hENT1 EXPRESSION</title><author xml:id="author-0000"><persName><forename type="first">Marcelo</forename><surname>Farías</surname></persName><affiliation><orgName type="laboratory">Cellular and Molecular Physiology Laboratory (CMPL)</orgName><orgName type="department">Department of Obstetrics and Gynaecology</orgName><orgName type="laboratory">Medical Research Centre (CIM)</orgName><orgName type="department">School of Medicine</orgName><orgName type="department">Faculty of Medicine</orgName><orgName type="institution">Pontificia Universidad Católica de Chile</orgName><address><addrLine>Santiago</addrLine><addrLine>Chile</addrLine><country key="CL" xml:lang="en">CHILE</country></address></affiliation></author><author xml:id="author-0001"><persName><forename type="first">Rody</forename><surname>San Martín</surname></persName><affiliation><orgName type="laboratory">Cellular and Molecular Physiology Laboratory (CMPL)</orgName><orgName type="department">Department of Obstetrics and Gynaecology</orgName><orgName type="laboratory">Medical Research Centre (CIM)</orgName><orgName type="department">School of Medicine</orgName><orgName type="department">Faculty of Medicine</orgName><orgName type="institution">Pontificia Universidad Católica de Chile</orgName><address><addrLine>Santiago</addrLine><addrLine>Chile</addrLine><country key="CL" xml:lang="en">CHILE</country></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">Carlos</forename><surname>Puebla</surname></persName><affiliation><orgName type="laboratory">Cellular and Molecular Physiology Laboratory (CMPL)</orgName><orgName type="department">Department of Obstetrics and Gynaecology</orgName><orgName type="laboratory">Medical Research Centre (CIM)</orgName><orgName type="department">School of Medicine</orgName><orgName type="department">Faculty of Medicine</orgName><orgName type="institution">Pontificia Universidad Católica de Chile</orgName><address><addrLine>Santiago</addrLine><addrLine>Chile</addrLine><country key="CL" xml:lang="en">CHILE</country></address></affiliation></author><author xml:id="author-0003"><persName><forename type="first">Jeremy D.</forename><surname>Pearson</surname></persName><affiliation><orgName type="division">Biomedical Sciences Division</orgName><address><addrLine>King's College London</addrLine><addrLine>University of London, London</addrLine><country key="GB" xml:lang="en">UNITED KINGDOM</country></address></affiliation></author><author xml:id="author-0004"><persName><forename type="first">Javier F.</forename><surname>Casado</surname></persName><affiliation><orgName type="laboratory">Departament de Bioquímica i Biologia Molecular</orgName><orgName type="institution">Universitat de Barcelona</orgName><address><addrLine>Barcelona</addrLine><addrLine>Spain</addrLine><country key="ES" xml:lang="en">SPAIN</country></address></affiliation></author><author xml:id="author-0005"><persName><forename type="first">Marçal</forename><surname>Pastor‐Anglada</surname></persName><affiliation><orgName type="laboratory">Departament de Bioquímica i Biologia Molecular</orgName><orgName type="institution">Universitat de Barcelona</orgName><address><addrLine>Barcelona</addrLine><addrLine>Spain</addrLine><country key="ES" xml:lang="en">SPAIN</country></address></affiliation></author><author xml:id="author-0006"><persName><forename type="first">Paola</forename><surname>Casanello</surname></persName><affiliation><orgName type="laboratory">Cellular and Molecular Physiology Laboratory (CMPL)</orgName><orgName type="department">Department of Obstetrics and Gynaecology</orgName><orgName type="laboratory">Medical Research Centre (CIM)</orgName><orgName type="department">School of Medicine</orgName><orgName type="department">Faculty of Medicine</orgName><orgName type="institution">Pontificia Universidad Católica de Chile</orgName><address><addrLine>Santiago</addrLine><addrLine>Chile</addrLine><country key="CL" xml:lang="en">CHILE</country></address></affiliation></author><author xml:id="author-0007" role="corresp"><persName><forename type="first">Luis</forename><surname>Sobrevia</surname></persName><email>sobrevia@med.puc.cl</email><affiliation><orgName type="laboratory">Cellular and Molecular Physiology Laboratory (CMPL)</orgName><orgName type="department">Department of Obstetrics and Gynaecology</orgName><orgName type="laboratory">Medical Research Centre (CIM)</orgName><orgName type="department">School of Medicine</orgName><orgName type="department">Faculty of Medicine</orgName><orgName type="institution">Pontificia Universidad Católica de Chile</orgName><address><addrLine>Santiago</addrLine><addrLine>Chile</addrLine><country key="CL" xml:lang="en">CHILE</country></address></affiliation></author><idno type="istex">9187712C25082F809449CE9A8F0BC79130B5A415</idno><idno type="ark">ark:/67375/WNG-C399R479-V</idno><idno type="DOI">10.1002/jcp.20680</idno><idno 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HUVEC from gestational diabetes exhibit reduced <hi rend="italic">SLC29A1</hi> promoter activity when transfected with pGL3‐hENT1<hi rend="superscript">−2154</hi> compared with pGL3‐hENT1<hi rend="superscript">−1114</hi> constructs, an effect blocked by <hi rend="italic">N</hi><hi rend="superscript">G</hi>‐nitro‐<hi rend="smallCaps">L</hi>‐arginine methyl ester (L‐NAME, NOS inhibitor), but unaltered by <hi rend="italic">S</hi>‐nitroso‐<hi rend="italic">N</hi>‐acetyl‐<hi rend="smallCaps">L</hi>,<hi rend="smallCaps">D</hi>‐penicillamine (SNAP, NO donor). In cells from gestational diabetes transfected with pGL3‐hENT1<hi rend="superscript">−2154</hi>, 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 <hi rend="italic">SLC29A1</hi> 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.</p></abstract><textClass><keywords rend="articleCategory"><term>Original Article</term></keywords><keywords rend="tocHeading1"><term>Original Articles</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc><revisionDesc><change when="2019-12-20" who="#istex" xml:id="pub2tei">formatting</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-C399R479-V/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1097-4652</doi><issn type="print">0021-9541</issn><issn type="electronic">1097-4652</issn><idGroup><id type="product" value="JCP"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="JOURNAL OF CELLULAR PHYSIOLOGY">Journal of Cellular Physiology</title><title type="short">J. 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Physiol.</title></titleGroup></publicationMeta><publicationMeta level="part" position="20"><doi origin="wiley" registered="yes">10.1002/jcp.v208:2</doi><numberingGroup><numbering type="journalVolume" number="208">208</numbering><numbering type="journalIssue">2</numbering></numberingGroup><coverDate startDate="2006-08">August 2006</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="220" status="forIssue"><doi origin="wiley" registered="yes">10.1002/jcp.20680</doi><idGroup><id type="unit" value="JCP20680"></id></idGroup><countGroup><count type="pageTotal" number="10"></count></countGroup><titleGroup><title type="articleCategory">Original Article</title><title type="tocHeading1">Original Articles</title></titleGroup><copyright ownership="publisher">Copyright © 2006 Wiley‐Liss, Inc.</copyright><eventGroup><event type="manuscriptReceived" date="2006-03-14"></event><event type="manuscriptAccepted" date="2006-04-06"></event><event type="publishedOnlineEarlyUnpaginated" date="2006-05-10"></event><event type="firstOnline" date="2006-05-10"></event><event type="publishedOnlineFinalForm" date="2006-05-24"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" date="2010-03-05"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-30"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-24"></event></eventGroup><numberingGroup><numbering type="pageFirst">451</numbering><numbering type="pageLast">460</numbering></numberingGroup><correspondenceTo>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, Chile.</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:JCP.JCP20680.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="5"></count><count type="tableTotal" number="2"></count><count type="referenceTotal" number="32"></count><count type="wordTotal" number="7428"></count></countGroup><titleGroup><title type="main" xml:lang="en">Nitric oxide reduces adenosine transporter ENT1 gene (<i>SLC29A1</i>) promoter activity in human fetal endothelium from gestational diabetes</title><title type="short" xml:lang="en">NITRIC OXIDE‐REDUCED hENT1 EXPRESSION</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Marcelo</givenNames><familyName>Farías</familyName></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Rody</givenNames><familyName>San Martín</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Carlos</givenNames><familyName>Puebla</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Jeremy D.</givenNames><familyName>Pearson</familyName></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Javier F.</givenNames><familyName>Casado</familyName></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Marçal</givenNames><familyName>Pastor‐Anglada</familyName></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Paola</givenNames><familyName>Casanello</familyName></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Luis</givenNames><familyName>Sobrevia</familyName></personName><contactDetails><email>sobrevia@med.puc.cl</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="CL" type="organization"><unparsedAffiliation>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, Chile</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="GB" type="organization"><unparsedAffiliation>Biomedical Sciences Division, King's College London, University of London, London</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="ES" type="organization"><unparsedAffiliation>Departament de Bioquímica i Biologia Molecular, Universitat de Barcelona, Barcelona, Spain</unparsedAffiliation></affiliation></affiliationGroup><fundingInfo><fundingAgency>FONDECYT</fundingAgency><fundingNumber>1030781</fundingNumber><fundingNumber>1030607</fundingNumber><fundingNumber>7050030</fundingNumber></fundingInfo><fundingInfo><fundingAgency>SAF</fundingAgency><fundingNumber>2005‐01259</fundingNumber></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>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 (<i>SLC29A1</i>) expression. HUVEC from gestational diabetes exhibit reduced <i>SLC29A1</i> promoter activity when transfected with pGL3‐hENT1<sup>−2154</sup> compared with pGL3‐hENT1<sup>−1114</sup> constructs, an effect blocked by <i>N</i><sup>G</sup>‐nitro‐<sc>L</sc>‐arginine methyl ester (L‐NAME, NOS inhibitor), but unaltered by <i>S</i>‐nitroso‐<i>N</i>‐acetyl‐<sc>L</sc>,<sc>D</sc>‐penicillamine (SNAP, NO donor). In cells from gestational diabetes transfected with pGL3‐hENT1<sup>−2154</sup>, 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 <i>SLC29A1</i> 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.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Nitric oxide reduces adenosine transporter ENT1 gene (SLC29A1) promoter activity in human fetal endothelium from gestational diabetes</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>NITRIC OXIDE‐REDUCED hENT1 EXPRESSION</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Nitric oxide reduces adenosine transporter ENT1 gene (SLC29A1) promoter activity in human fetal endothelium from gestational diabetes</title></titleInfo><name type="personal"><namePart type="given">Marcelo</namePart><namePart type="family">Farías</namePart><affiliation>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, Chile</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Rody</namePart><namePart type="family">San Martín</namePart><affiliation>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, Chile</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Carlos</namePart><namePart type="family">Puebla</namePart><affiliation>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, Chile</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jeremy D.</namePart><namePart type="family">Pearson</namePart><affiliation>Biomedical Sciences Division, King's College London, University of London, London</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Javier F.</namePart><namePart type="family">Casado</namePart><affiliation>Departament de Bioquímica i Biologia Molecular, Universitat de Barcelona, Barcelona, Spain</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Marçal</namePart><namePart type="family">Pastor‐Anglada</namePart><affiliation>Departament de Bioquímica i Biologia Molecular, Universitat de Barcelona, Barcelona, Spain</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Paola</namePart><namePart type="family">Casanello</namePart><affiliation>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, Chile</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Luis</namePart><namePart type="family">Sobrevia</namePart><affiliation>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, Chile</affiliation><affiliation>E-mail: sobrevia@med.puc.cl</affiliation><affiliation>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, Chile.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2006-08</dateIssued><dateCaptured encoding="w3cdtf">2006-03-14</dateCaptured><dateValid encoding="w3cdtf">2006-04-06</dateValid><copyrightDate encoding="w3cdtf">2006</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="figures">5</extent><extent unit="tables">2</extent><extent unit="references">32</extent><extent unit="words">7428</extent></physicalDescription><abstract 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.</abstract><note type="funding">FONDECYT - No. 1030781; No. 1030607; No. 7050030; </note><note type="funding">SAF - No. 2005‐01259; </note><relatedItem type="host"><titleInfo><title>Journal of Cellular Physiology</title></titleInfo><titleInfo type="abbreviated"><title>J. Cell. 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