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The present study was designed to investigate the involvement of BMPR2 in the protective effect of fluoxetine against monocrotaline (MCT)-induced endothelial apoptosis in rats. Models of pulmonary arterial hypertension in rats were established by a single intraperitoneal injection of MCT (60\u00a0mg\/kg). Fluoxetine (2\u00a0and 10\u00a0mg\/kg) was intragastrically administered once a day. After 21\u00a0days, MCT caused pulmonary hypertension, right ventricular hypertrophy, and pulmonary vascular remodeling and significantly reduced the BMPR2 expression in lungs and pulmonary arteries. Fluoxetine dose-dependently inhibited MCT-induced pulmonary arterial hypertension and effectively protected the lungs against MCT-induced endothelial apoptosis, reduction in the number of alveolar sacs, and loss of the pulmonary small vessels. Fluoxetine reversed the expression of cyclic guanosine 3\u2032,5\u2032-monophosphate-dependent kinase \u0406, BMPR2, phospho-Smad1, \u03b2-catenin, and reduced the expression of caspase 3 in rat lungs. These findings suggest that BMPR2 is probably involved in the protective effect of fluoxetine against MCT-induced endothelial apoptosis in rats.<\/jats:p>","DOI":"10.1139\/y11-024","type":"journal-article","created":{"date-parts":[[2011,6,3]],"date-time":"2011-06-03T07:23:17Z","timestamp":1307085797000},"page":"345-354","source":"Crossref","is-referenced-by-count":6,"title":["Involvement of BMPR2 in the protective effect of fluoxetine against monocrotaline-induced endothelial apoptosis in rats"],"prefix":"10.1139","volume":"89","author":[{"given":"Yun","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Clinical Pharmacology, China Medical University, No.\u00a092, 2nd North Road, Heping District, Shenyang 110001, P.R. 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