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.
Url:
DOI: 10.1002/jcp.21347
Links to Exploration step
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<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. Physiol. 215: 645–656, 2008. © 2007 Wiley‐Liss, Inc.</div>
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<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>
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<json:string>San ´ Martın and Sobrevia, 2006</json:string>
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<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>
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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>
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<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>
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<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>
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<noteGroup><note xml:id="fn1"><p>Paola Casanello and Luis Sobrevia contributed equally to this study.</p>
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<role><roleTerm type="text">author</roleTerm>
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<name type="personal"><namePart type="given">Andrea</namePart>
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<name type="personal"><namePart type="given">Claudio</namePart>
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<affiliation>Current Address: Faculty of Pharmacy, Universidad de Concepción, Chile.</affiliation>
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<name type="personal"><namePart type="given">Bernardo</namePart>
<namePart type="family">Krause</namePart>
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<affiliation>Basic Sciences Department, Faculty of Biological Sciences, Universidad del Bío‐Bío, Chile</affiliation>
<role><roleTerm type="text">author</roleTerm>
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<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>
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</role>
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<name type="personal"><namePart type="given">Paola</namePart>
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<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>
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<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>
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