Título:
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Reduced adenosine uptake and its contribution to signaling that mediates profibrotic activation in renal tubular epithelial cells: implication in diabetic nephropathy.
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Autor/a:
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Kretschmar, Catalina; Oyarzún, Carlos; Villablanca, Cristopher; Jaramillo, Catherinne; Alarcón, Sebastián; Perez, Gustavo; Díaz-Encarnación, Montserrat M.M.; Pastor Anglada, Marçal; Garrido, Wallys; Quezada, Claudia; San Martín, Rody
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Otros autores:
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Universitat de Barcelona |
Abstract:
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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. |
Materia(s):
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-Diabetis -Cèl·lules epitelials -Adenosina -Diabetes -Epithelial cells -Adenosine |
Derechos:
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cc-by (c) Kretschmar, Catalina et al., 2016
http://creativecommons.org/licenses/by/3.0/es |
Tipo de documento:
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Artículo Artículo - Versión publicada |
Editor:
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Public Library of Science (PLoS)
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