{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T07:43:14Z","timestamp":1791186194506,"version":"4.1.0"},"reference-count":72,"publisher":"Rockefeller University Press","issue":"2","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2014,2,10]]},"abstract":"<jats:p>Idiopathic pulmonary arterial hypertension (PAH [IPAH]) is an insidious and potentially fatal disease linked to a mutation or reduced expression of bone morphogenetic protein receptor 2 (BMPR2). Because intravascular inflammatory cells are recruited in IPAH pathogenesis, we hypothesized that reduced BMPR2 enhances production of the potent chemokine granulocyte macrophage colony-stimulating factor (GM-CSF) in response to an inflammatory perturbation. When human pulmonary artery (PA) endothelial cells deficient in BMPR2 were stimulated with tumor necrosis factor (TNF), a twofold increase in GM-CSF was observed and related to enhanced messenger RNA (mRNA) translation. The mechanism was associated with disruption of stress granule formation. Specifically, loss of BMPR2 induced prolonged phospho-p38 mitogen-activated protein kinase (MAPK) in response to TNF, and this increased GADD34\u2013PP1 phosphatase activity, dephosphorylating eukaryotic translation initiation factor (eIF2\u03b1), and derepressing GM-CSF mRNA translation. Lungs from IPAH patients versus unused donor controls revealed heightened PA expression of GM-CSF co-distributing with increased TNF and expanded populations of hematopoietic and endothelial GM-CSF receptor \u03b1 (GM-CSFR\u03b1)\u2013positive cells. Moreover, a 3-wk infusion of GM-CSF in mice increased hypoxia-induced PAH, in association with increased perivascular macrophages and muscularized distal arteries, whereas blockade of GM-CSF repressed these features. Thus, reduced BMPR2 can subvert a stress granule response, heighten GM-CSF mRNA translation, increase inflammatory cell recruitment, and exacerbate PAH.<\/jats:p>","DOI":"10.1084\/jem.20111741","type":"journal-article","created":{"date-parts":[[2014,1,21]],"date-time":"2014-01-21T02:35:13Z","timestamp":1390271713000},"page":"263-280","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":147,"title":["Reduced BMPR2 expression induces GM-CSF translation and macrophage recruitment in humans and mice to exacerbate pulmonary hypertension"],"prefix":"10.1084","volume":"211","author":[{"given":"Hirofumi","family":"Sawada","sequence":"first","affiliation":[{"name":"The Vera Moulton Wall Center for Pulmonary Vascular Disease 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"Department of Pediatrics 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"Department of Surgery 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"Department of Microbiology and Immunology 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"Department of Medicine 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"The Vera Moulton Wall Center for Pulmonary Vascular Disease 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"Department of Pediatrics 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"Department of Surgery 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"Department of Microbiology and Immunology 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"Department of Medicine 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"The Vera Moulton Wall Center for Pulmonary Vascular Disease 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"Department of Pediatrics 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"Department of Surgery 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"Department of Microbiology and Immunology 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"Department of Medicine 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6"},{"name":"Department of Surgery 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"Department of Microbiology and Immunology 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"Department of Medicine 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"The Vera Moulton Wall Center for Pulmonary Vascular Disease 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"Department of Pediatrics 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"Department of Surgery 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"Department of Microbiology and Immunology 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"Department of Medicine 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"The Vera Moulton Wall Center for Pulmonary Vascular Disease 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"Department of Pediatrics 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"Department of Surgery 1 , 2 , 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6"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Edda","family":"Spiekerkoetter","sequence":"additional","affiliation":[{"name":"The Vera Moulton Wall Center for Pulmonary Vascular Disease 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"Department of Pediatrics 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"Department of Surgery 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"Department of Microbiology and Immunology 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"Department of Medicine 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"The Vera Moulton Wall Center for Pulmonary Vascular Disease 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"Department of Pediatrics 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"Department of Surgery 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"Department of Microbiology and Immunology 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"Department of Medicine 1 , 2 , 3 , 4 , 5 , and 6"},{"name":"Cardiovascular 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