Browsing by Author "Aguayo, Claudio"

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    High D-Glucose reduces SLC29A1 promoter activity and adenosine transport involving specific protein 1 in human umbilical vein endothelium
    (WILEY, 2008) Puebla, Carlos; Farias, Marcelo; Gonzalez, Marcelo; Vecchiola, Andrea; Aguayo, Claudio; Krause, Bernardo; Pastor Anglada, Marcal; Casanello, Paola; Sobrevia, Luis
    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. N-G-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 4 alpha-phorbol 12,13-didecanoate (4 alpha PDD, 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.
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    Potential role of A2B adenosine receptors on proliferation/migration of fetal endothelium derived from preeclamptic pregnancies
    (2014) Acurio, Jesenia; Troncoso, Felipe; Bertoglia, Patricio; Salomon, Carlos; Aguayo, Claudio; Sobrevía Luarte, Luis Alberto; Escudero, Carlos
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    Pro-angiogenic Role of Insulin: From Physiology to Pathology
    (2017) Escudero, Carlos A.; Herlitz, Kurt; Troncoso, Felipe; Guevara, Katherine; Acurio, Jesenia; Godoy Sánchez, Alejandro Samuel; Aguayo, Claudio; González, Marcelo