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Does BMPR2 Mutation Disrupt Pulmonary Vasculogenesis?*

Trina K. Jeffery, PhD; Paul D. Upton, PhD; X. Yang, PhD; M. Southwood, BSc; L. Long, PhD; R. C. Trembath, FRCP; Nicholas W. Morrell, MD
Author and Funding Information

*From the Department of Medicine, University of Cambridge School of Clinical Medicine, Addenbrooke’s and Papworth Hospitals, Cambridge, UK.

Correspondence to: Nicholas W. Morrell, MD, Division of Respiratory Medicine, Department of Medicine, Box 157, Addenbrooke’s Hospital, Hills Rd, Cambridge, CB2 2QQ, UK; e-mail: nwm23@cam.ac.uk



Chest. 2005;128(6_suppl):602S. doi:10.1378/chest.128.6_suppl.602S
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Mutations in the gene encoding the bone morphogenetic protein type II receptor (BMPR2) cause familial primary pulmonary hypertension, although the precise mechanism remains obscure. We previously found that expression of BMPR-II is predominantly localized to endothelial cells in lung tissue. In addition, mice deficient in the bone morphogenetic protein (BMP)-restricted signaling intermediary, Smad5, exhibit defects in angiogenesis. To begin to clarify the role of BMP signaling in pulmonary vasculogenesis/angiogenesis, we studied the expression of BMP-2/BMP-4, BMPR2, Smad1, and phospho-Smad1 in developing human embryos and fetuses.

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