Figure 2.

Formoterol inhibits chronic hypoxia-induced human PAVSM cell proliferation. Cells grown under chronic hypoxia (1% O₂) or normoxia (21% O₂) for 7 days were serum-deprived for 48 h, treated with 10 μM (R,R)-, (S,S)-, racemic formoterol, or diluent (A), or 0.1, 1, 10 ng/ml PDGF, or diluent in the absence or presence of 10 μM (R,R) and racemic formoterol (B), and then DNA synthesis analysis using the BrdU incorporation assay was performed. DNA synthesis was measured as a percentage of the BrdU-positive cells per total number of cells. Data are means ± SE by ANOVA (Bonferroni-Dunn) from three independent experiments; n = 3 for each experimental condition. A minimum of 200 cells per condition were analyzed in each experiment. A: *p < 0.01 for diluent-treated cells under normoxia vs. hypoxia and for racemic formoterol vs. (R,R) formoterol under normoxia; **p < 0.001 for racemic formoterol vs. (R,R) formoterol under hypoxia. B: *p < 0.001 for hypoxia vs. normoxia; **p < 0.01 for diluent vs. (R,R) formoterol under normoxia; for diluent vs. racemic formoterol under hypoxia; and for 0.1 ng/ml PDGF vs. 0.1 ng/ml PDGF + racemic formoterol under hypoxia; ***p < 0.001 for 0.1 ng/ml PDGF vs. 0.1 ng/ml PDGF + (R,R) formoterol under normoxia; for diluent vs. (R,R) formoterol under hypoxia; and for 0.1 ng/ml PDGF + (R,R) formoterol under hypoxia.