Please use this identifier to cite or link to this item: http://hdl.handle.net/2445/104525
Title: Reduced adenosine uptake and its contribution to signaling that mediates profibrotic activation in renal tubular epithelial cells: implication in diabetic nephropathy.
Author: 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
Keywords: Diabetis
Cèl·lules epitelials
Adenosina
Diabetes
Epithelial cells
Adenosine
Issue Date: 25-Jan-2016
Publisher: Public Library of Science (PLoS)
Abstract: 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.
Note: Reproducció del document publicat a: https://doi.org/10.1371/journal.pone.0147430
It is part of: PLoS One, 2016, vol. 11, num. 1, p. e0147430
Related resource: https://doi.org/10.1371/journal.pone.0147430
URI: http://hdl.handle.net/2445/104525
ISSN: 1932-6203
Appears in Collections:Articles publicats en revistes (Bioquímica i Biomedicina Molecular)

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