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 4
Antiproliferative effects of BMP-2 and the PPARγ agonist rosiglitazone on PDGF-BB–induced proliferation of human wild-type and BMP-RII mutant PASMCs. Control PASMCs were isolated from surgical resection specimens derived from patients undergoing lobectomy or pneumonectomy for suspected lung tumor. Additional peripheral pulmonary arteries (<1–2 mm external diameter) were obtained from a patient undergoing heart-lung transplantation for FPAH and known to harbor a mutation (W9X) in BMP-RII. The nature of the BMP-RII mutation, cell isolation, culture techniques, and cell counts are described in Methods and in Figure 1. HPASMCs were incubated for 48 hours in starvation media (0.1% FBS) and then stimulated with PDGF-BB (20 ng/ml) for 72 hours. BMP-2 (10 ng/ml) or rosiglitazone (1 μM) were added to quiescent cells 30 minutes prior to PDGF-BB stimulation. Bars represent mean ± SEM (n = 3). **P < 0.01; ***P < 0.001 as indicated; ANOVA with Bonferroni’s multiple comparison test. The number of PDGF-BB–stimulated cells was significantly higher than that of untreated control cells (P < 0.001).