Figure 10. Renal hypoxia in mice with tissue-specific deletion of Adora2b.

(A) Adora2b reporter mice (Adora2b-KO/β-gal–knock-in mice) were exposed to 30 minutes of renal ischemia and 24 hours of reperfusion (+I) or underwent sham operation (–I). Renal tissues were stained for β-gal as an indicator of the Adora2b gene promoter, which drives expression of the reporter gene (original magnification, ×400; 1 representative image of 3 is shown). Small arrows indicate the glomerulus. Bold arrows indicate Adora2b staining. (B) Staining for tissue hypoxia utilizing pimonidazole compounds that are retained in hypoxic tissues. Wild-type mice were treated with dipyridamole (0.25 mg i.v.; I+DIP) or vehicle (I–DIP; control: sham operation) and were exposed to 30 minutes of ischemia. Mice were injected with pimonidazole 5 minutes after renal ischemia, and staining was performed after 20 minutes of reperfusion (original magnification, ×100; 1 representative image of 3 is shown). (C) Similar experimental setup in Adora2b^loxP/loxPVE-cadherin–Cre⁺ mice (1 representative image of 3 is shown).