The muscularization of non-muscular pulmonary arterioles is an important pathological featureof hypoxic pulmonary vascular remodeling.However,the origin of the cells involved in this process is stillnot well understood.The present study was undertaken to test the hypothesis that transforming growthfactor-β1 (TGF-β1) can induce transdifferentiation of fibroblasts into myofibroblasts,which might play akey role in the muscularization of non-muscular pulmonary arterioles.It was found that mean pulmonaryarterial pressure increased significantly after 7 d of hypoxia.Pulmonary artery remodeling index and rightventricular hypertrophy became evident after 14 d of hypoxia.The distribution of nonmuscular,partiallymuscular,and muscular vessels was significantly different after 7 d of hypoxia.Immunocytochemistryresults demonstrated that the expression of co-smooth muscle actin was increased in intra-acinar pulmonaryarteries with increasing hypoxic time.TGF-β1 mRNA expression in pulmonary arterial walls was increasedsignificantly after 14 d of hypoxia,but showed no obvious changes after 3 or 7 d of hypoxia.In pulmonarytunica adventitia and tunica media,TGF-β1 protein staining was poorly positive in control rats,but wasmarkedly enhanced after 3 d of hypoxia,reaching its peak after 7 d Of hypoxia.The myofibroblast phenotypewas confirmed by electron microscopy,which revealed microfilaments and a well-developed rough endo-plasmic reticulum.Taken together,our results suggested that TGF-β1 induces transdifferentiation of fibro-blasts into myofibroblasts,which is important in hypoxic pulmonary vascular remodeling. The muscularization of non-muscular pulmonary arterioles is an important pathological feature of hypoxic pulmonary vascular remodeling. Although the origin of the cells involved in this process is still well understood. The present study was undertaken to test the hypothesis that transforming growth factor-β1 (TGF -β1) can induce transdifferentiation of fibroblasts into myofibroblasts, which might play a key role in the muscularization of non-muscular pulmonary arterioles. It was found that mean pulmonary artery pressure increased significantly after 7 d of hypoxia. Pulmonary artery remodeling index and right ventricular hypertrophy became evident after 14 d of hypoxia. the distribution of nonmuscular, partially muscular, and muscular vessels was significantly different after 7 d of hypoxia. Immunocytochemistry results showed that the expression of co-smooth muscle actin was increased in intra-acinar pulmonary artery with increasing hypoxic time. TGF- β1 mRNA expression in pulmonary arteria l walls was increased sificly after 14 d of hypoxia, but showed no obvious changes after 3 or 7 d of hypoxia.In pulmonary tunica adventitia and tunica media, TGF-β1 protein staining was poorly positive in control rats, but wasmarkedly enhanced after 3 d of hypoxia , its peak after 7 d Of hypoxia. myofibroblast phenotype was confirmed by electron microscopy, which showed microfilaments and a well-developed rough endo-plasmic reticulum. Taken together, our results suggested that TGF-β1 induces transdifferentiation of fibro-blasts into myofibroblasts , which is important in hypoxic pulmonary vascular remodeling.