Objectives To test the hypotheses that bone morphogenetic protein(BMP) signaling pathway components are expressed in arterial endothelial cells (ECs) and that BMP signaling influences endothelial cell(EC) proliferation. Methods We used cell culture and RT-PCR to determined mRNA expression of BMP receptors (BMPR)-IA, -IB, and II, Smads 1, 4, 5, 6, and 7, and in cultured human coronary artery ECs at baseline and after stimulation with BMP2 (300 ng/mL for 6 hr), non-radioactive cell proliferation to examine cell proliferation. Results Proteasome inhibition has been previously shown to enhance BMP signaling by preventing degradation of BMP pathway components. Therefore, identical experiments were also performed in the presence of the proteasome inhibitor epoxomicin. ECs expressed mRNA for BMPRs IA and II, Smads 1, 4, 5, 6, 7, and stimulation with either BMP2 or epoxomicin resulted in a significant increase in EC proliferation measured after 48 hours in a dose-dependent fashion. Proliferation was accompanied by a marked increase in proliferating cell nuclear antigen (PCNA) expression. Toxicity was observed at high doses of epoxomicin. Conclusions All major BMP signaling molecules are expressed by vascular ECs and expression of these are affected by both BMP2 and epoxomicin. BMP2 may regulate EC proliferation, suggesting a possible role in vascular homeostasis and vascular pathologies involving EC denudation or proliferation. Objectives To test the hypotheses that bone morphogenetic protein (BMP) signaling pathway components are expressed in arterial endothelial cells (ECs) and that BMP signaling influences endothelial cell (EC) proliferation. Methods We used cell culture and RT-PCR to determined mRNA expression of BMP receptors (BMPR) -IA, -IB, and II, Smads 1, 4, 5, 6, and 7, and in cultured human coronary artery ECs at baseline and after stimulation with BMP2 (300 ng / mL for 6 hr) Results Proteasome inhibition has been previously shown to enhance BMP signaling by preventing degradation of BMP pathway components. Thus, both experiments performed also on the proteasome inhibitor epoxomicin. ECs expressed mRNA for BMPRs IA and II, Smads 1, 4, 5, 6, 7, and stimulation with either BMP2 or epoxomicin resulted in a significant increase in EC proliferation measured after 48 hours in a dose-dependent fashion. Proliferati on was accompanied by a marked increase in proliferating cell nuclear antigen (PCNA) expression. Toxicity was observed at high doses of epoxomicin. Conclusions All major BMP signaling molecules are expressed by vascular ECs and expression of these are affected by both BMP2 and epoxomicin. BMP2 may regulate EC proliferation, suggesting a possible role in vascular homeostasis and vascular pathologies involving EC denudation or proliferation.