Objective: We investigated the effects and possible mechanism of intravenous transplantation of syngenic bone marrow-derived mononuclear cells (BMMNCs) on pulmonary artery hypertension (PAH) induced by monocrotaline (MCT). Methods: MCT of 80 mg/kg-weight was administrated to C57BL/6 mice, and it induced PAH 4 weeks later. BMMNCs harvested from syngenic donor mice were injected intravenously to those mice 4 weeks after MCT-administration. Right ventricle/septum-left ventricle weight ratio, the number of small pulmonary artery, and medial thickness of PA were observed. Western immnoblotting of the lung tissue was performed to observe vascular endothelial growth factor (VEGF) expression at one week after BMMNCs transplantation. VEGFR-2 inhibitor was administrated to the PAH mice simultaneously with BMMNCs transplantation. Results: RV/S+LV weight ratio increased, the number of PA decreased, and medial thickness increased significantly 28 days after MCT-injection compared to those of vehicle-injected mice, respectively (0.296±0.04 vs 0.203±0.02; 5.1±1.7 vs 20.9±4.8; 21.5%±5.2% vs 7.5%±2.1%, p<0.01). These indices of MCT-injected mice improved significantly 28 days after BMMNCs transplantation compared to those mice of 8 weeks after MCT/PBS-injection, respectively (0.22±0.02 vs 0.31±0.02; 17.1±2.6 vs 8.2±1.7; 7.7%±2.2% vs 20%±2.1%, p<0.01). However, BMMNCs were not incorporated into the lung during one week after the transplantation. Upregulation of VEGF was observed significantly in the lung tissue one week after transplantation. Moreover improvement of PAH was inhibited by administration of VEGFR-2 inhibitor. Conclusions: These results indicate that intravenous transplantation of syngenic BMMNCs improves MCT-induced PAH through VEGF-VEGFR system. Intravenous transplantation of syngenic BMMNCs has the potential as a new therapeutic option for PAH.