An antiproliferative BMP-2/PPARγ/apoE axis in human and murine SMCs and its role in pulmonary hypertension
J. Clin. Invest. Georg Hansmann, et al. 118:1846 doi:10.1172/JCI32503 [Go to this article.]

Figure 3
BMP-2 and rosiglitazone inhibit PDGF-BB–mediated ERK phosphorylation (A and C), and concomitant BMP-2 and PDGF-BB stimulation increases PPARγ DNA binding (B), in HPASMCs. Cells were preincubated with BMP-2 (10 ng/ml) for 30 minutes (A and B) or rosiglitazone (1 μM) for 24 hours (C), followed by PDGF-BB (20 ng/ml) stimulation for 10 minutes (A and B) or 5–60 minutes. (C) Western immunoblotting and PPARγ DNA binding assays are described in Methods and Figure 2. For protein levels in cell fractions (A) or cell lysates (C), bars represent mean ± SEM (n = 3 each). In C, all samples are compared with the DMSO control. For the PPARγ DNA binding assay (B), bars represent median ± SEM of triplicate measurements of 1 representative experiment of 3 independent experiments with similar results. *P < 0.05; **P < 0.01 versus control; ANOVA with Dunnett’s post-hoc test.