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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
The purine nucleoside adenosine has established anti-inflammatory effects whilst also being reported to promote organ fibrosis by signaling through the adenosine A2a and A2b receptors (encoded by the Adora2a and Adora2b genes, respectively). The adenosine A2b receptor has low affinity and is only activated by adenosine concentrations achieved during organ injury. We reasoned that these properties would render the adenosine A2b receptor a promising candidate to target in the development of a kidney antifibrotic therapy. Accordingly, here we examined the consequences of deletion of the adenosine A2b receptor from fibroblasts in mice with obstructive uropathy caused by unilateral ureteral obstruction (UUO), a well-established model of kidney inflammation and fibrosis.
Knockdown of Adora2b was achieved with siRNA in mouse embryonic fibroblasts (MEFs). Adora2bfl/fl mice were bred with Col1a2CreER+ mice to generate tamoxifen-inducible fibroblast-specific adenosine A2b receptor knockout mice (A2BFibKO). Adora2b knockout was achieved by feeding mice a tamoxifen-containing diet and kidney expression changes and histological parameters were compared with those in tamoxifen-fed Adora2bfl/fl mice (A2BCtrl) 14 days after sham or UUO surgery.
Adora2b mRNA levels were increased >3-fold in UUO kidneys in comparison to kidneys from sham-operated mice. Knockdown of Adora2b diminished upregulation of mRNA levels of the profibrotic growth factor Ccn2 induced by transforming growth factor-beta in MEFs. Fibroblast-specific adenosine A2b receptor knockout similarly diminished upregulation of Ccn2, and Col1a1, in UUO mice. Conversely, upregulation of mRNA levels of the basement membrane collagen Col4a1, the inflammatory cytokine Il6 and the markers of tubule injury Postn and Havcr1 were augmented with adenosine A2b receptor knockout in UUO mice. These gene expression changes were reflected in a numerical but non-significant reduction in interstitial fibrosis, with persistent tubule epithelial programmed cell death and macrophage accumulation. Expression of the higher affinity Adora2a remained elevated in UUO kidneys.
Knockout of the adenosine A2b receptor from fibroblasts causes transcriptional changes in obstructed kidneys that are characterized by attenuation in upregulation of some fibrotic genes and augmentation in upregulation of some inflammatory genes and injury markers; without altering overall kidney structure. The gene expression changes that occur with Adora2b knockout reflect both the direct consequences of adenosine A2b receptor absence, and indirect compensatory responses occurring in fibroblasts and other kidney cells. The results highlight the complexity of adenosine receptor targeting as a means for attenuating kidney fibrosis and improving outcomes in kidney disease.
