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. 2013 Feb 15;304(8):L549–L561. doi: 10.1152/ajplung.00081.2012

Fig. 4.

Fig. 4.

Effect of BQ-123 treatment on the hypoxia-induced increase in HIF-1α and PHD2. PASMCs were exposed to control (20% O2) or hypoxic (4% O2) conditions in the absence or presence of BQ-123 (10 μM) for 60 h. Protein (n = 3–4; A) and mRNA (n = 3; B) levels of HIF-1α and PHD2 relative to cells treated with BQ-123 under normoxic conditions. C: HIF-1 target genes induced by hypoxia in PASMCs in the absence and presence of BQ-123 (n = 3–4). D: HIF-1α protein accumulation in response to short-term, severe hypoxia (4 h; 1% O2) in the absence and presence of BQ-123. Data are normalized to cyclophilin B or actin for mRNA and protein, respectively, and expressed relative to 20% O2. *P < 0.05 from 20% O2. E: HIF-1α mRNA levels in endothelium-denuded pulmonary arteries from rats treated with either saline (vehicle; n = 4 each) or BQ-123 (1 mg/kg; n = 3–4 each) and exposed to normoxia (room air) or hypoxia (FiO2 = 10%) for 24 h. F: PHD2 mRNA levels in endothelium-denuded pulmonary arteries from normoxic and hypoxic rats treated with either saline (n = 4 each) or BQ-123 (n = 3–4 each). mRNA data for HIF-1α and PHD2 are normalized to 18s and expressed relative to saline-treated normoxia. *P < 0.05 from saline-treated room air. For all bar graphs, mean ± SE values are shown.