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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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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.
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KRETSCHMAR, Catalina, et al. Reduced adenosine uptake and its contribution to signaling that mediates profibrotic activation in renal tubular epithelial cells: implication in diabetic nephropathy. PLoS One. 2016. Vol. 11, num. 1, pags. e0147430. ISSN 1932-6203. [consulted: 19 of August of 2026]. Available at: https://hdl.handle.net/2445/104525