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               <dc:title>Reduced adenosine uptake and its contribution to signaling that mediates profibrotic activation in renal tubular epithelial cells: implication in diabetic nephropathy.</dc:title>
               <dc:creator>Kretschmar, Catalina</dc:creator>
               <dc:creator>Oyarzún, Carlos</dc:creator>
               <dc:creator>Villablanca, Cristopher</dc:creator>
               <dc:creator>Jaramillo, Catherinne</dc:creator>
               <dc:creator>Alarcón, Sebastián</dc:creator>
               <dc:creator>Perez, Gustavo</dc:creator>
               <dc:creator>Díaz-Encarnación, Montserrat M. M.</dc:creator>
               <dc:creator>Pastor Anglada, Marçal</dc:creator>
               <dc:creator>Garrido, Wallys</dc:creator>
               <dc:creator>Quezada, Claudia</dc:creator>
               <dc:creator>San Martín, Rody</dc:creator>
               <dc:subject>Diabetis</dc:subject>
               <dc:subject>Cèl·lules epitelials</dc:subject>
               <dc:subject>Adenosina</dc:subject>
               <dc:subject>Diabetes</dc:subject>
               <dc:subject>Epithelial cells</dc:subject>
               <dc:subject>Adenosine</dc:subject>
               <dc:description>Altered nucleoside levels may be linked to pathogenic signaling through adenosine recep- tors. We hypothesized that adenosine dysregulation contributes to fibrosis in diabetic kid- ney disease. Our findings indicate that high glucose levels and experimental diabetes decreased uptake activity through the equilibrative nucleoside transporter 1 (ENT1) in proxi- mal tubule cells. In addition, a correlation between increased plasma content of adenosine and a marker of renal fibrosis in diabetic rats was evidenced. At the cellular level, exposure of HK2 cells to high glucose, TGF- β and the general adenosine receptor agonist NECA, induced the expression of profibrotic cell activation markers α -SMA and fibronectin. These effects can be avoided by using a selective antagonist of the adenosine A 3 receptor subtype in vitro. Furthermore, induction of fibrosis marker α -SMA was prevented by the A 3 receptor antagonist in diabetic rat kidneys. In conclusion, we evidenced the contribution of purinergic signaling to renal fibrosis in experimental diabetic nephropathy.</dc:description>
               <dc:date>2016-12-07T13:11:58Z</dc:date>
               <dc:date>2016-12-07T13:11:58Z</dc:date>
               <dc:date>2016-01-25</dc:date>
               <dc:date>2016-12-07T13:12:03Z</dc:date>
               <dc:type>info:eu-repo/semantics/article</dc:type>
               <dc:type>info:eu-repo/semantics/publishedVersion</dc:type>
               <dc:relation>Reproducció del document publicat a: https://doi.org/10.1371/journal.pone.0147430</dc:relation>
               <dc:relation>PLoS One, 2016, vol. 11, num. 1, p. e0147430</dc:relation>
               <dc:relation>https://doi.org/10.1371/journal.pone.0147430</dc:relation>
               <dc:rights>cc-by (c) Kretschmar, Catalina et al., 2016</dc:rights>
               <dc:rights>http://creativecommons.org/licenses/by/3.0/es</dc:rights>
               <dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
               <dc:publisher>Public Library of Science (PLoS)</dc:publisher>
               <dc:source>Articles publicats en revistes (Bioquímica i Biomedicina Molecular)</dc:source>
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