Role of HIF-1 and CREB in CD73 hypoxia-inducibility. (a) Confluent BAE monolayers were exposed to mock treatment (Ctl), HIF-1α sense oligonucleotides (S), or HIF-1α antisense oligonucleotides (AS) for 48 hours. Total protein was solubilized, and HIF-1α expression was examined by Western blot. Nx, normoxia. (b) Confluent BAE monolayers were transiently transfected with plasmids expressing sequence corresponding to truncations at the 5′ end (pGL2^0.57NT, bp –518 to +63) in the presence or absence of HIF-1α sense or antisense oligonucleotides. Twelve hours later, cells were exposed to hypoxia for 48 hours and assessed for luciferase activity. Data are mean ± SEM from three separate experiments. **P < 0.01. (c) Confluent BAE monolayers were transiently transfected with plasmids expressing sequence corresponding to truncations at the 5′ end (pGL2^0.57NT, bp –518 to +63) or plasmids encoding HIF-1 or CRE mutations, as indicated. Twelve hours later, cells were exposed to hypoxia or normoxia for 48 hours and assessed for luciferase activity. All transfections were normalized to cotransfected β-galactosidase activity. Data are mean ± SEM from three separate experiments. *P < 0.025 compared with the corresponding nonmutated control; **P < 0.01 compared with normoxia.