The major conclusion of our study is that, in our model of hypoxic pulmonary artery remodeling without endothelial disruption, the adhesive bone marrow-derived CD45- CD73+ CD90+ MSCs are not significantly integrated in the parietal wall after repeated intravenous infusion whereas it has been described in systemic vascular remodeling such graft vasculopathy and arteriosclerosis with endothelial progenitor cells. This evidence concerns the gene NT5E and arteriosclerosis disorder.