Kretschmar, CatalinaOyarzún, CarlosVillablanca, CristopherJaramillo, CatherinneAlarcón, SebastiánPerez, GustavoDíaz-Encarnación, Montserrat M. M.Pastor Anglada, MarçalGarrido, WallysQuezada, ClaudiaSan Martín, Rody2016-12-072016-12-072016-01-251932-6203https://hdl.handle.net/2445/104525Altered 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.20 p.application/pdfengcc-by (c) Kretschmar, Catalina et al., 2016http://creativecommons.org/licenses/by/3.0/esDiabetisCèl·lules epitelialsAdenosinaDiabetesEpithelial cellsAdenosineinfo:eu-repo/semantics/article6633092016-12-07info:eu-repo/semantics/openAccess26808537