Pretreatment with a selective COX-2 inhibitor, NS-398, increased PHE-induced contraction (Fig. 4D), but reduced ACH-induced relaxation in arteries treated with BMEPCs (Fig. 4E), thereby suggesting that up-regulation of COX-2 was responsible for the improved effect of BMEPCs on PAH relaxation. Here, PTGS2 is linked to pulmonary arterial hypertension.