Altered growth responses of muscle cells from patients pulmonary artery smooth with primary pulmonary hypertension to transforming growth factor-beta(1) and bone morphogenetic proteins

N W Morrell, X D Yang, P D Upton, K B Jourdan, N Morgan, K K Sheares, R C Trembath

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398 Citations (Scopus)

Abstract

Background-Mutations in the type II receptor for bone morphogenetic protein (BMPR-II), a receptor member of the transforming growth factor-beta (TGF-beta) superfamily, underlie many cases of familial and sporadic primary pulmonary hypertension (PPH). We postulated that pulmonary artery smooth muscle cells (PASMCs) from patients with PPH might demonstrate abnormal growth responses to TGF-beta superfamily members. Methods and Results-For studies of H-3-thymidine incorporation or cell proliferation, PASMCs (passages 4 to 8) were derived from main pulmonary arteries. In control cells, 24-hour incubation with TGF-beta (1) (10 ng/mL) or bone morphogenetic protein (BMP)-2, -4, and -7 (100 ng/mL) inhibited basal and serum-stimulated H-3-thymidine incorporation, and TGF-beta (1) and BMPs inhibited the proliferation of serum-stimulated PASMCs. In contrast, TGF-beta (1) stimulated H-3-thymidine incorporation (200%; P
Original languageEnglish
Pages (from-to)790 - 795
Number of pages6
JournalCirculation (Baltimore)
Volume104
Issue number7
DOIs
Publication statusPublished - 2001

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