High D‐glucose reduces SLC29A1 promoter activity and adenosine transport involving specific protein 1 in human umbilical vein endothelium
Identifieur interne : 002386 ( Istex/Corpus ); précédent : 002385; suivant : 002387High D‐glucose reduces SLC29A1 promoter activity and adenosine transport involving specific protein 1 in human umbilical vein endothelium
Auteurs : Carlos Puebla ; Marcelo Farías ; Marcelo González ; Andrea Vecchiola ; Claudio Aguayo ; Bernardo Krause ; Marçal Pastor-Anglada ; Paola Casanello ; Luis SobreviaSource :
- Journal of Cellular Physiology [ 0021-9541 ] ; 2008-06.
Abstract
High D‐glucose reduces human equilibrative nucleoside transporter 1 (hENT1)‐mediated adenosine uptake involving endothelial nitric oxide synthase (eNOS), mitogen‐activated protein (MAP) kinase kinases 1 and 2/MAP kinases p42/44 (MEK/ERKs), and protein kinase C (PKC) activation in human umbilical vein endothelium (HUVEC). Since NO represses SLC29A1 gene (hENT1) promoter activity we studied whether D‐glucose‐reduced hENT1‐adenosine transport results from lower SLC29A1 expression in HUVEC primary cultures. HUVEC incubation (24 h) with high D‐glucose (25 mM) reduced hENT1‐adenosine transport and pGL3‐hENT1−1114 construct SLC29A1 reporter activity compared with normal D‐glucose (5 mM). High D‐glucose also reduced pGL3‐hENT1−1114 reporter activity compared with cells transfected with pGL3‐hENT1−795 construct. NG‐nitro‐L‐arginine methyl ester (L‐NAME, NOS inhibitor), PD‐98059 (MEK1/2 inhibitor), and/or calphostin C (PKC inhibitor) blocked D‐glucose effects. Insulin (1 nM) and phorbol 12‐myristate 13‐acetate (PMA, 100 nM, PKC activator), but not 4α‐phorbol 12,13‐didecanoate (4αPDD, 100 nM, PMA less active analogue) reduced hENT1‐adenosine transport. L‐NAME and PD‐98059 blocked insulin effects. L‐NAME, PD‐98059, and calphostin C increased hENT1 expression without altering protein or mRNA stability. High D‐glucose increased Sp1 transcription factor protein abundance and binding to SLC29A1 promoter, phenomena blocked by L‐NAME, PD‐98059, and calphostin C. Sp1 overexpression reduced SLC29A1 promoter activity in normal D‐glucose, an effect reversed by L‐NAME and further reduced by S‐nitroso‐N‐acetyl‐L,D‐penicillamine (SNAP, NO donor) in high D‐glucose. Thus, reduced hENT1‐mediated adenosine transport in high D‐glucose may result from increased Sp1 binding to SLC29A1 promoter down‐regulating hENT1 expression. This phenomenon depends on eNOS, MEK/ERKs, and PKC activity, suggesting potential roles for these molecules in hyperglycemia‐associated endothelial dysfunction. J. Cell. Physiol. 215: 645–656, 2008. © 2007 Wiley‐Liss, Inc.
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DOI: 10.1002/jcp.21347
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Research Laboratory (PRL), 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) and Perinatal Research Laboratory (PRL), 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></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:7A8E46B18F42530AF3E771E482066C4C2C2CB025</idno><date when="2008" year="2008">2008</date><idno type="doi">10.1002/jcp.21347</idno><idno type="url">https://api.istex.fr/ark:/67375/WNG-2DD8VCM3-7/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">002386</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">002386</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main">High D‐glucose reduces SLC29A1 promoter activity and adenosine transport involving specific protein 1 in human umbilical vein endothelium</title><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) and Perinatal Research Laboratory (PRL), 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="Farias, Marcelo" sort="Farias, Marcelo" uniqKey="Farias M" first="Marcelo" last="Farías">Marcelo Farías</name><affiliation><mods:affiliation>Cellular and Molecular Physiology Laboratory (CMPL) and Perinatal Research Laboratory (PRL), 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="Gonzalez, Marcelo" sort="Gonzalez, Marcelo" uniqKey="Gonzalez M" first="Marcelo" last="González">Marcelo González</name><affiliation><mods:affiliation>Cellular and Molecular Physiology Laboratory (CMPL) and Perinatal Research Laboratory (PRL), 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="Vecchiola, Andrea" sort="Vecchiola, Andrea" uniqKey="Vecchiola A" first="Andrea" last="Vecchiola">Andrea Vecchiola</name><affiliation><mods:affiliation>Cellular and Molecular Physiology Laboratory (CMPL) and Perinatal Research Laboratory (PRL), 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="Aguayo, Claudio" sort="Aguayo, Claudio" uniqKey="Aguayo C" first="Claudio" last="Aguayo">Claudio Aguayo</name><affiliation><mods:affiliation>Cellular and Molecular Physiology Laboratory (CMPL) and Perinatal Research Laboratory (PRL), 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>Current Address: Faculty of Pharmacy, Universidad de Concepción, Chile.</mods:affiliation></affiliation></author><author><name sortKey="Krause, Bernardo" sort="Krause, Bernardo" uniqKey="Krause B" first="Bernardo" last="Krause">Bernardo Krause</name><affiliation><mods:affiliation>Cellular and Molecular Physiology Laboratory (CMPL) and Perinatal Research Laboratory (PRL), 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>Basic Sciences Department, Faculty of Biological Sciences, Universidad del Bío‐Bío, Chile</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>Department of Biochemistry and Molecular Biology, Institute of Biomedicine, (IBUB), University of Barcelona, CIBER EHD, 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) and Perinatal Research Laboratory (PRL), 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) and Perinatal Research Laboratory (PRL), 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">215</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="645">645</biblScope><biblScope unit="page" to="656">656</biblScope><biblScope unit="page-count">12</biblScope><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2008-06">2008-06</date></imprint><idno type="ISSN">0021-9541</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0021-9541</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">High D‐glucose reduces human equilibrative nucleoside transporter 1 (hENT1)‐mediated adenosine uptake involving endothelial nitric oxide synthase (eNOS), mitogen‐activated protein (MAP) kinase kinases 1 and 2/MAP kinases p42/44 (MEK/ERKs), and protein kinase C (PKC) activation in human umbilical vein endothelium (HUVEC). Since NO represses SLC29A1 gene (hENT1) promoter activity we studied whether D‐glucose‐reduced hENT1‐adenosine transport results from lower SLC29A1 expression in HUVEC primary cultures. HUVEC incubation (24 h) with high D‐glucose (25 mM) reduced hENT1‐adenosine transport and pGL3‐hENT1−1114 construct SLC29A1 reporter activity compared with normal D‐glucose (5 mM). High D‐glucose also reduced pGL3‐hENT1−1114 reporter activity compared with cells transfected with pGL3‐hENT1−795 construct. NG‐nitro‐L‐arginine methyl ester (L‐NAME, NOS inhibitor), PD‐98059 (MEK1/2 inhibitor), and/or calphostin C (PKC inhibitor) blocked D‐glucose effects. Insulin (1 nM) and phorbol 12‐myristate 13‐acetate (PMA, 100 nM, PKC activator), but not 4α‐phorbol 12,13‐didecanoate (4αPDD, 100 nM, PMA less active analogue) reduced hENT1‐adenosine transport. L‐NAME and PD‐98059 blocked insulin effects. L‐NAME, PD‐98059, and calphostin C increased hENT1 expression without altering protein or mRNA stability. High D‐glucose increased Sp1 transcription factor protein abundance and binding to SLC29A1 promoter, phenomena blocked by L‐NAME, PD‐98059, and calphostin C. Sp1 overexpression reduced SLC29A1 promoter activity in normal D‐glucose, an effect reversed by L‐NAME and further reduced by S‐nitroso‐N‐acetyl‐L,D‐penicillamine (SNAP, NO donor) in high D‐glucose. Thus, reduced hENT1‐mediated adenosine transport in high D‐glucose may result from increased Sp1 binding to SLC29A1 promoter down‐regulating hENT1 expression. This phenomenon depends on eNOS, MEK/ERKs, and PKC activity, suggesting potential roles for these molecules in hyperglycemia‐associated endothelial dysfunction. J. Cell. 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(CMPL) and Perinatal Research Laboratory (PRL), 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>Marcelo González</name><affiliations><json:string>Cellular and Molecular Physiology Laboratory (CMPL) and Perinatal Research Laboratory (PRL), 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>Andrea Vecchiola</name><affiliations><json:string>Cellular and Molecular Physiology Laboratory (CMPL) and Perinatal Research Laboratory (PRL), 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>Claudio Aguayo</name><affiliations><json:string>Cellular and Molecular Physiology Laboratory (CMPL) and Perinatal Research Laboratory (PRL), 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>Current Address: Faculty of Pharmacy, Universidad de Concepción, Chile.</json:string></affiliations></json:item><json:item><name>Bernardo Krause</name><affiliations><json:string>Cellular and Molecular Physiology Laboratory (CMPL) and Perinatal Research Laboratory (PRL), 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>Basic Sciences Department, Faculty of Biological Sciences, Universidad del Bío‐Bío, Chile</json:string></affiliations></json:item><json:item><name>Marçal Pastor‐Anglada</name><affiliations><json:string>Department of Biochemistry and Molecular Biology, Institute of Biomedicine, (IBUB), University of Barcelona, CIBER EHD, Barcelona, Spain</json:string></affiliations></json:item><json:item><name>Paola Casanello</name><affiliations><json:string>Cellular and Molecular Physiology Laboratory (CMPL) and Perinatal Research Laboratory (PRL), 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) and Perinatal Research Laboratory (PRL), 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>JCP21347</json:string></articleId><arkIstex>ark:/67375/WNG-2DD8VCM3-7</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>High D‐glucose reduces human equilibrative nucleoside transporter 1 (hENT1)‐mediated adenosine uptake involving endothelial nitric oxide synthase (eNOS), mitogen‐activated protein (MAP) kinase kinases 1 and 2/MAP kinases p42/44 (MEK/ERKs), and protein kinase C (PKC) activation in human umbilical vein endothelium (HUVEC). Since NO represses SLC29A1 gene (hENT1) promoter activity we studied whether D‐glucose‐reduced hENT1‐adenosine transport results from lower SLC29A1 expression in HUVEC primary cultures. HUVEC incubation (24 h) with high D‐glucose (25 mM) reduced hENT1‐adenosine transport and pGL3‐hENT1−1114 construct SLC29A1 reporter activity compared with normal D‐glucose (5 mM). High D‐glucose also reduced pGL3‐hENT1−1114 reporter activity compared with cells transfected with pGL3‐hENT1−795 construct. NG‐nitro‐L‐arginine methyl ester (L‐NAME, NOS inhibitor), PD‐98059 (MEK1/2 inhibitor), and/or calphostin C (PKC inhibitor) blocked D‐glucose effects. Insulin (1 nM) and phorbol 12‐myristate 13‐acetate (PMA, 100 nM, PKC activator), but not 4α‐phorbol 12,13‐didecanoate (4αPDD, 100 nM, PMA less active analogue) reduced hENT1‐adenosine transport. L‐NAME and PD‐98059 blocked insulin effects. L‐NAME, PD‐98059, and calphostin C increased hENT1 expression without altering protein or mRNA stability. High D‐glucose increased Sp1 transcription factor protein abundance and binding to SLC29A1 promoter, phenomena blocked by L‐NAME, PD‐98059, and calphostin C. Sp1 overexpression reduced SLC29A1 promoter activity in normal D‐glucose, an effect reversed by L‐NAME and further reduced by S‐nitroso‐N‐acetyl‐L,D‐penicillamine (SNAP, NO donor) in high D‐glucose. Thus, reduced hENT1‐mediated adenosine transport in high D‐glucose may result from increased Sp1 binding to SLC29A1 promoter down‐regulating hENT1 expression. This phenomenon depends on eNOS, MEK/ERKs, and PKC activity, suggesting potential roles for these molecules in hyperglycemia‐associated endothelial dysfunction. J. Cell. Physiol. 215: 645–656, 2008. © 2007 Wiley‐Liss, Inc.</abstract><qualityIndicators><score>10</score><pdfWordCount>8944</pdfWordCount><pdfCharCount>56452</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>12</pdfPageCount><pdfPageSize>592 x 789 pts</pdfPageSize><pdfWordsPerPage>745</pdfWordsPerPage><pdfText>true</pdfText><refBibsNative>true</refBibsNative><abstractWordCount>259</abstractWordCount><abstractCharCount>2049</abstractCharCount><keywordCount>0</keywordCount></qualityIndicators><title>High D‐glucose reduces SLC29A1 promoter activity and adenosine transport involving specific protein 1 in human umbilical vein endothelium</title><pmid><json:string>18064606</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>215</volume><issue>3</issue><pages><first>645</first><last>656</last><total>12</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>28S</json:string><json:string>2008</json:string></date><geogName><json:string>San</json:string><json:string>Sawa</json:string></geogName><orgName><json:string>PRL</json:string><json:string>Roche Diagnostics</json:string><json:string>Medical Research Centre</json:string><json:string>Chile, Santiago, Chile Ponti</json:string><json:string>Spain High</json:string><json:string>Clontech, Palo Alto</json:string><json:string>Chile, Comision</json:string><json:string>Department of Obstetrics and Gynaecology</json:string><json:string>University of Barcelona</json:string><json:string>Tecnologica</json:string><json:string>Institute of Biomedicine</json:string><json:string>BioRad Laboratories</json:string><json:string>CIM</json:string><json:string>Biochem</json:string><json:string>Hospital Cl</json:string><json:string>Santa Cruz Biotechnology</json:string><json:string>Basic Sciences Department, Faculty of Biological Sciences, Universidad</json:string><json:string>Neurochem</json:string><json:string>Calbiochem</json:string><json:string>Biochemicals</json:string><json:string>Tecnologica, Chile</json:string><json:string>Wiley-Liss, Inc</json:string><json:string>Department of Biochemistry and Molecular Biology</json:string><json:string>Chile, Vice-Rector</json:string><json:string>Amersham</json:string><json:string>GIBCO Life Technologies</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Luis Sobrevia</json:string><json:string>Claudio Aguayo</json:string><json:string>J. 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Acurio</json:string><json:string>Nat Med</json:string><json:string>Assay</json:string><json:string>Nat Neurosci</json:string><json:string>La Jolla</json:string><json:string>Paola Casanello</json:string></persName><placeName><json:string>Bad Wildbad</json:string><json:string>Bradford</json:string><json:string>Carlsbad</json:string><json:string>Germany</json:string><json:string>Hertfordshire</json:string><json:string>Tropea</json:string><json:string>SY</json:string><json:string>Chile</json:string><json:string>UK</json:string><json:string>IN</json:string><json:string>Buckinghamshire</json:string><json:string>Mannheim</json:string><json:string>Madison</json:string><json:string>Wessendorf</json:string><json:string>Santiago</json:string><json:string>Barcelona</json:string><json:string>Santa Cruz</json:string><json:string>Puri</json:string><json:string>CA</json:string><json:string>WI</json:string><json:string>PUEBLA</json:string><json:string>Indianapolis</json:string><json:string>Puebla</json:string><json:string>Spain</json:string></placeName><ref_url><json:string>http://www.genomatix.de/ products/matinspector/matinspector</json:string><json:string>http://motif.genome.jp</json:string></ref_url><ref_bibl><json:string>Wang et al., 1999</json:string><json:string>San ´ Martın and Sobrevia, 2006</json:string><json:string>Puebla et al., 2007</json:string><json:string>Starzynski et al., 2006</json:string><json:string>Park et al., 1997</json:string><json:string>Fiuza et al., 2003</json:string><json:string>Casanello et al., 2007</json:string><json:string>Soler et al., 2000</json:string><json:string>Aguayo et al., 2005</json:string><json:string>Oomen et al., 2002</json:string><json:string>Deves and Boyd, 1998</json:string><json:string>Sakowicz et al., 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type="main">High D‐glucose reduces SLC29A1 promoter activity and adenosine transport involving specific protein 1 in human umbilical vein endothelium</title><title level="a" type="short" xml:lang="en">Sp1‐DEPENDENT GLUCOSE INHIBITION OF hENT1</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><licence>Copyright © 2007 Wiley‐Liss, Inc.</licence></availability><date type="published" when="2008-06"></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">High D‐glucose reduces SLC29A1 promoter activity and adenosine transport involving specific protein 1 in human umbilical vein endothelium</title><title level="a" type="short" xml:lang="en">Sp1‐DEPENDENT GLUCOSE INHIBITION OF hENT1</title><author xml:id="author-0000"><persName><forename type="first">Carlos</forename><surname>Puebla</surname></persName><affiliation><orgName type="laboratory">Cellular and Molecular Physiology Laboratory (CMPL) and Perinatal Research Laboratory (PRL)</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">Marcelo</forename><surname>Farías</surname></persName><affiliation><orgName type="laboratory">Cellular and Molecular Physiology Laboratory (CMPL) and Perinatal Research Laboratory (PRL)</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">Marcelo</forename><surname>González</surname></persName><affiliation><orgName type="laboratory">Cellular and Molecular Physiology Laboratory (CMPL) and Perinatal Research Laboratory (PRL)</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">Andrea</forename><surname>Vecchiola</surname></persName><affiliation><orgName type="laboratory">Cellular and Molecular Physiology Laboratory (CMPL) and Perinatal Research Laboratory (PRL)</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-0004"><persName><forename type="first">Claudio</forename><surname>Aguayo</surname></persName><affiliation><orgName type="laboratory">Cellular and Molecular Physiology Laboratory (CMPL) and Perinatal Research Laboratory (PRL)</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><affiliation><orgName type="department">Faculty of Pharmacy</orgName><orgName type="institution">Universidad de Concepción</orgName><address><addrLine>Chile.</addrLine><country key="CL" xml:lang="en">CHILE</country></address></affiliation></author><author xml:id="author-0005"><persName><forename type="first">Bernardo</forename><surname>Krause</surname></persName><affiliation><orgName type="laboratory">Cellular and Molecular Physiology Laboratory (CMPL) and Perinatal Research Laboratory (PRL)</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><affiliation><orgName type="division">Basic Sciences Department</orgName><orgName type="laboratory">Faculty of Biological Sciences</orgName><orgName type="institution">Universidad del Bío‐Bío</orgName><address><addrLine>Chile</addrLine><country key="CL" xml:lang="en">CHILE</country></address></affiliation></author><author xml:id="author-0006"><persName><forename type="first">Marçal</forename><surname>Pastor‐Anglada</surname></persName><affiliation><orgName type="laboratory">Department of Biochemistry and Molecular Biology</orgName><orgName type="institution">Institute of Biomedicine</orgName><orgName type="institution">(IBUB)</orgName><orgName type="institution">University of Barcelona</orgName><orgName type="institution">CIBER EHD</orgName><address><addrLine>Barcelona</addrLine><addrLine>Spain</addrLine><country key="ES" xml:lang="en">SPAIN</country></address></affiliation></author><author xml:id="author-0007"><persName><forename type="first">Paola</forename><surname>Casanello</surname></persName><affiliation><orgName type="laboratory">Cellular and Molecular Physiology Laboratory (CMPL) and Perinatal Research Laboratory (PRL)</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-0008" 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) and Perinatal Research Laboratory (PRL)</orgName><orgName type="department">Department of Obstetrics and Gynaecology</orgName><orgName type="laboratory">Medical Research Centre (CIM)</orgName><orgName type="department">School of 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<ref target="http://www.tei-c.org/">We use TEI</ref></desc></application></appInfo></encodingDesc><profileDesc><abstract xml:lang="en" style="main"><head>Abstract</head><p>High <hi rend="smallCaps">D</hi>‐glucose reduces human equilibrative nucleoside transporter 1 (hENT1)‐mediated adenosine uptake involving endothelial nitric oxide synthase (eNOS), mitogen‐activated protein (MAP) kinase kinases 1 and 2/MAP kinases p42/44 (MEK/ERKs), and protein kinase C (PKC) activation in human umbilical vein endothelium (HUVEC). Since NO represses <hi rend="italic">SLC29A1</hi> gene (hENT1) promoter activity we studied whether <hi rend="smallCaps">D</hi>‐glucose‐reduced hENT1‐adenosine transport results from lower <hi rend="italic">SLC29A1</hi> expression in HUVEC primary cultures. HUVEC incubation (24 h) with high <hi rend="smallCaps">D</hi>‐glucose (25 mM) reduced hENT1‐adenosine transport and pGL3‐hENT1<hi rend="superscript">−1114</hi> construct <hi rend="italic">SLC29A1</hi> reporter activity compared with normal <hi rend="smallCaps">D</hi>‐glucose (5 mM). High <hi rend="smallCaps">D</hi>‐glucose also reduced pGL3‐hENT1<hi rend="superscript">−1114</hi> reporter activity compared with cells transfected with pGL3‐hENT1<hi rend="superscript">−795</hi> construct. <hi rend="italic">N</hi><hi rend="superscript">G</hi>‐nitro‐<hi rend="smallCaps">L</hi>‐arginine methyl ester (<hi rend="smallCaps">L</hi>‐NAME, NOS inhibitor), PD‐98059 (MEK1/2 inhibitor), and/or calphostin C (PKC inhibitor) blocked <hi rend="smallCaps">D</hi>‐glucose effects. Insulin (1 nM) and phorbol 12‐myristate 13‐acetate (PMA, 100 nM, PKC activator), but not 4α‐phorbol 12,13‐didecanoate (4αPDD, 100 nM, PMA less active analogue) reduced hENT1‐adenosine transport. <hi rend="smallCaps">L</hi>‐NAME and PD‐98059 blocked insulin effects. <hi rend="smallCaps">L</hi>‐NAME, PD‐98059, and calphostin C increased hENT1 expression without altering protein or mRNA stability. High <hi rend="smallCaps">D</hi>‐glucose increased Sp1 transcription factor protein abundance and binding to <hi rend="italic">SLC29A1</hi> promoter, phenomena blocked by <hi rend="smallCaps">L</hi>‐NAME, PD‐98059, and calphostin C. Sp1 overexpression reduced <hi rend="italic">SLC29A1</hi> promoter activity in normal <hi rend="smallCaps">D</hi>‐glucose, an effect reversed by <hi rend="smallCaps">L</hi>‐NAME and further reduced 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 high <hi rend="smallCaps">D</hi>‐glucose. Thus, reduced hENT1‐mediated adenosine transport in high <hi rend="smallCaps">D</hi>‐glucose may result from increased Sp1 binding to <hi rend="italic">SLC29A1</hi> promoter down‐regulating hENT1 expression. This phenomenon depends on eNOS, MEK/ERKs, and PKC activity, suggesting potential roles for these molecules in hyperglycemia‐associated endothelial dysfunction. J. Cell. Physiol. 215: 645–656, 2008. © 2007 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-2DD8VCM3-7/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. Cell. Physiol.</title></titleGroup></publicationMeta><publicationMeta level="part" position="30"><doi origin="wiley" registered="yes">10.1002/jcp.v215:3</doi><numberingGroup><numbering type="journalVolume" number="215">215</numbering><numbering type="journalIssue">3</numbering></numberingGroup><coverDate startDate="2008-06">June 2008</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="100" status="forIssue"><doi origin="wiley" registered="yes">10.1002/jcp.21347</doi><idGroup><id type="unit" value="JCP21347"></id></idGroup><countGroup><count type="pageTotal" number="12"></count></countGroup><titleGroup><title type="articleCategory">Original Article</title><title type="tocHeading1">Original Articles</title></titleGroup><copyright ownership="publisher">Copyright © 2007 Wiley‐Liss, Inc.</copyright><eventGroup><event type="manuscriptReceived" date="2007-07-28"></event><event type="manuscriptAccepted" date="2007-10-12"></event><event type="publishedOnlineEarlyUnpaginated" date="2007-12-06"></event><event type="firstOnline" date="2007-12-06"></event><event type="publishedOnlineFinalForm" date="2008-03-24"></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="2014-10-23"></event></eventGroup><numberingGroup><numbering type="pageFirst">645</numbering><numbering type="pageLast">656</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.JCP21347.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="7"></count><count type="tableTotal" number="1"></count><count type="referenceTotal" number="50"></count><count type="wordTotal" number="9769"></count></countGroup><titleGroup><title type="main" xml:lang="en">High <sc>D</sc>‐glucose reduces <i>SLC29A1</i> promoter activity and adenosine transport involving specific protein 1 in human umbilical vein endothelium<link href="#fn1"></link></title><title type="short" xml:lang="en">Sp1‐DEPENDENT GLUCOSE INHIBITION OF hENT1</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Carlos</givenNames><familyName>Puebla</familyName></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Marcelo</givenNames><familyName>Farías</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Marcelo</givenNames><familyName>González</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Andrea</givenNames><familyName>Vecchiola</familyName></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1" currentRef="#curr1"><personName><givenNames>Claudio</givenNames><familyName>Aguayo</familyName></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Bernardo</givenNames><familyName>Krause</familyName></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Marçal</givenNames><familyName>Pastor‐Anglada</familyName></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Paola</givenNames><familyName>Casanello</familyName></personName></creator><creator xml:id="au9" 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) and Perinatal Research Laboratory (PRL), 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="CL" type="organization"><unparsedAffiliation>Basic Sciences Department, Faculty of Biological Sciences, Universidad del Bío‐Bío, Chile</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="ES" type="organization"><unparsedAffiliation>Department of Biochemistry and Molecular Biology, Institute of Biomedicine, (IBUB), University of Barcelona, CIBER EHD, Barcelona, Spain</unparsedAffiliation></affiliation><affiliation xml:id="curr1" countryCode="CL"><unparsedAffiliation>Faculty of Pharmacy, Universidad de Concepción, Chile.</unparsedAffiliation></affiliation></affiliationGroup><fundingInfo><fundingAgency>Fondo Nacional de Desarrollo Científico y Tecnológica, Chile (FONDECYT)</fundingAgency><fundingNumber>1070865</fundingNumber><fundingNumber>7070249</fundingNumber></fundingInfo><fundingInfo><fundingAgency>Comisión Nacional de Investigación Científica y Tecnológica, Chile (CONICYT)</fundingAgency><fundingNumber>23070213</fundingNumber></fundingInfo><fundingInfo><fundingAgency>Vice‐Rectoría Adjunta de Investigación y Doctorado, Pontificia Universidad Católica de Chile (VRAID)</fundingAgency><fundingNumber>BM16/2007</fundingNumber><fundingNumber>BM14/2007</fundingNumber></fundingInfo><fundingInfo><fundingAgency>Agencia Española de Cooperación Internacional, Spain (AECI)</fundingAgency><fundingNumber>A/5484/06</fundingNumber><fundingNumber>SAF2005‐01259</fundingNumber></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>High <sc>D</sc>‐glucose reduces human equilibrative nucleoside transporter 1 (hENT1)‐mediated adenosine uptake involving endothelial nitric oxide synthase (eNOS), mitogen‐activated protein (MAP) kinase kinases 1 and 2/MAP kinases p42/44 (MEK/ERKs), and protein kinase C (PKC) activation in human umbilical vein endothelium (HUVEC). Since NO represses <i>SLC29A1</i> gene (hENT1) promoter activity we studied whether <sc>D</sc>‐glucose‐reduced hENT1‐adenosine transport results from lower <i>SLC29A1</i> expression in HUVEC primary cultures. HUVEC incubation (24 h) with high <sc>D</sc>‐glucose (25 mM) reduced hENT1‐adenosine transport and pGL3‐hENT1<sup>−1114</sup> construct <i>SLC29A1</i> reporter activity compared with normal <sc>D</sc>‐glucose (5 mM). High <sc>D</sc>‐glucose also reduced pGL3‐hENT1<sup>−1114</sup> reporter activity compared with cells transfected with pGL3‐hENT1<sup>−795</sup> construct. <i>N</i><sup>G</sup>‐nitro‐<sc>L</sc>‐arginine methyl ester (<sc>L</sc>‐NAME, NOS inhibitor), PD‐98059 (MEK1/2 inhibitor), and/or calphostin C (PKC inhibitor) blocked <sc>D</sc>‐glucose effects. Insulin (1 nM) and phorbol 12‐myristate 13‐acetate (PMA, 100 nM, PKC activator), but not 4α‐phorbol 12,13‐didecanoate (4αPDD, 100 nM, PMA less active analogue) reduced hENT1‐adenosine transport. <sc>L</sc>‐NAME and PD‐98059 blocked insulin effects. <sc>L</sc>‐NAME, PD‐98059, and calphostin C increased hENT1 expression without altering protein or mRNA stability. High <sc>D</sc>‐glucose increased Sp1 transcription factor protein abundance and binding to <i>SLC29A1</i> promoter, phenomena blocked by <sc>L</sc>‐NAME, PD‐98059, and calphostin C. Sp1 overexpression reduced <i>SLC29A1</i> promoter activity in normal <sc>D</sc>‐glucose, an effect reversed by <sc>L</sc>‐NAME and further reduced by <i>S</i>‐nitroso‐<i>N</i>‐acetyl‐<sc>L</sc>,<sc>D</sc>‐penicillamine (SNAP, NO donor) in high <sc>D</sc>‐glucose. Thus, reduced hENT1‐mediated adenosine transport in high <sc>D</sc>‐glucose may result from increased Sp1 binding to <i>SLC29A1</i> promoter down‐regulating hENT1 expression. This phenomenon depends on eNOS, MEK/ERKs, and PKC activity, suggesting potential roles for these molecules in hyperglycemia‐associated endothelial dysfunction. J. Cell. Physiol. 215: 645–656, 2008. © 2007 Wiley‐Liss, Inc.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>Paola Casanello and Luis Sobrevia contributed equally to this study.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>High D‐glucose reduces SLC29A1 promoter activity and adenosine transport involving specific protein 1 in human umbilical vein endothelium</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Sp1‐DEPENDENT GLUCOSE INHIBITION OF hENT1</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>High D‐glucose reduces SLC29A1 promoter activity and adenosine transport involving specific protein 1 in human umbilical vein endothelium</title></titleInfo><name type="personal"><namePart type="given">Carlos</namePart><namePart type="family">Puebla</namePart><affiliation>Cellular and Molecular Physiology Laboratory (CMPL) and Perinatal Research Laboratory (PRL), 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">Marcelo</namePart><namePart type="family">Farías</namePart><affiliation>Cellular and Molecular Physiology Laboratory (CMPL) and Perinatal Research Laboratory (PRL), 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">Marcelo</namePart><namePart type="family">González</namePart><affiliation>Cellular and Molecular Physiology Laboratory (CMPL) and Perinatal Research Laboratory (PRL), 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">Andrea</namePart><namePart type="family">Vecchiola</namePart><affiliation>Cellular and Molecular Physiology Laboratory (CMPL) and Perinatal Research Laboratory (PRL), 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">Claudio</namePart><namePart type="family">Aguayo</namePart><affiliation>Cellular and Molecular Physiology Laboratory (CMPL) and Perinatal Research Laboratory (PRL), Department of Obstetrics and Gynaecology, Medical Research Centre (CIM), School of Medicine, Faculty of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile</affiliation><affiliation>Current Address: Faculty of Pharmacy, Universidad de Concepción, Chile.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Bernardo</namePart><namePart type="family">Krause</namePart><affiliation>Cellular and Molecular Physiology Laboratory (CMPL) and Perinatal Research Laboratory (PRL), Department of Obstetrics and Gynaecology, Medical Research Centre (CIM), School of Medicine, Faculty of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile</affiliation><affiliation>Basic Sciences Department, Faculty of Biological Sciences, Universidad del Bío‐Bío, Chile</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Marçal</namePart><namePart type="family">Pastor‐Anglada</namePart><affiliation>Department of Biochemistry and Molecular Biology, Institute of Biomedicine, (IBUB), University of Barcelona, CIBER EHD, 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) and Perinatal Research Laboratory (PRL), 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) and Perinatal Research Laboratory (PRL), 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">2008-06</dateIssued><dateCaptured encoding="w3cdtf">2007-07-28</dateCaptured><dateValid encoding="w3cdtf">2007-10-12</dateValid><copyrightDate encoding="w3cdtf">2008</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="figures">7</extent><extent unit="tables">1</extent><extent unit="references">50</extent><extent unit="words">9769</extent></physicalDescription><abstract lang="en">High D‐glucose reduces human equilibrative nucleoside transporter 1 (hENT1)‐mediated adenosine uptake involving endothelial nitric oxide synthase (eNOS), mitogen‐activated protein (MAP) kinase kinases 1 and 2/MAP kinases p42/44 (MEK/ERKs), and protein kinase C (PKC) activation in human umbilical vein endothelium (HUVEC). Since NO represses SLC29A1 gene (hENT1) promoter activity we studied whether D‐glucose‐reduced hENT1‐adenosine transport results from lower SLC29A1 expression in HUVEC primary cultures. HUVEC incubation (24 h) with high D‐glucose (25 mM) reduced hENT1‐adenosine transport and pGL3‐hENT1−1114 construct SLC29A1 reporter activity compared with normal D‐glucose (5 mM). High D‐glucose also reduced pGL3‐hENT1−1114 reporter activity compared with cells transfected with pGL3‐hENT1−795 construct. NG‐nitro‐L‐arginine methyl ester (L‐NAME, NOS inhibitor), PD‐98059 (MEK1/2 inhibitor), and/or calphostin C (PKC inhibitor) blocked D‐glucose effects. Insulin (1 nM) and phorbol 12‐myristate 13‐acetate (PMA, 100 nM, PKC activator), but not 4α‐phorbol 12,13‐didecanoate (4αPDD, 100 nM, PMA less active analogue) reduced hENT1‐adenosine transport. L‐NAME and PD‐98059 blocked insulin effects. L‐NAME, PD‐98059, and calphostin C increased hENT1 expression without altering protein or mRNA stability. High D‐glucose increased Sp1 transcription factor protein abundance and binding to SLC29A1 promoter, phenomena blocked by L‐NAME, PD‐98059, and calphostin C. Sp1 overexpression reduced SLC29A1 promoter activity in normal D‐glucose, an effect reversed by L‐NAME and further reduced by S‐nitroso‐N‐acetyl‐L,D‐penicillamine (SNAP, NO donor) in high D‐glucose. Thus, reduced hENT1‐mediated adenosine transport in high D‐glucose may result from increased Sp1 binding to SLC29A1 promoter down‐regulating hENT1 expression. This phenomenon depends on eNOS, MEK/ERKs, and PKC activity, suggesting potential roles for these molecules in hyperglycemia‐associated endothelial dysfunction. J. Cell. Physiol. 215: 645–656, 2008. © 2007 Wiley‐Liss, Inc.</abstract><note type="content">*Paola Casanello and Luis Sobrevia contributed equally to this study.</note><note type="funding">Fondo Nacional de Desarrollo Científico y Tecnológica, Chile (FONDECYT) - No. 1070865; No. 7070249; </note><note type="funding">Comisión Nacional de Investigación Científica y Tecnológica, Chile (CONICYT) - No. 23070213; </note><note type="funding">Vice‐Rectoría Adjunta de Investigación y Doctorado, Pontificia Universidad Católica de Chile (VRAID) - No. BM16/2007; No. BM14/2007; </note><note type="funding">Agencia Española de Cooperación Internacional, Spain (AECI) - No. A/5484/06; No. SAF2005‐01259; </note><relatedItem type="host"><titleInfo><title>Journal of Cellular Physiology</title></titleInfo><titleInfo type="abbreviated"><title>J. Cell. 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