Increased expression of thrombospondin-1 in the interstitium of immature lungs exposed to hyperoxic or inflammatory stimuli in addition to local release and activation of thrombospondin-1 from platelets traversing the pulmonary microvascular bed is a reasonable mechanism for how thrombospondin-1 may contribute to the reduced angiogenesis that occurs in BPD, possibly connecting to pathways shown in Figure 3 via inflammatory signals. This evidence concerns the gene THBS1 and bronchopulmonary dysplasia.