TY - JOUR T1 - Imatinib inhibits bone marrow-derived c-kit<sup>+</sup> cell mobilisation in hypoxic pulmonary hypertension JF - European Respiratory Journal JO - Eur Respir J SP - 1209 LP - 1211 DO - 10.1183/09031936.00052210 VL - 36 IS - 5 AU - N. Gambaryan AU - F. Perros AU - D. Montani AU - S. Cohen-Kaminsky AU - G.M. Mazmanian AU - M. Humbert Y1 - 2010/11/01 UR - http://erj.ersjournals.com/content/36/5/1209.abstract N2 - To the Editors:We read with great interest the review by Fadini et al. 1 in the European Respiratory Journal discussing the role of bone marrow (BM)-derived stem cells and endothelial progenitors in pulmonary hypertension (PH). This topic is very relevant to pulmonary vascular medicine, indeed pioneering studies demonstrated that haematopoietic progenitor cells can be recruited in the pulmonary artery adventitia of neonatal animals with hypoxic PH 2. In addition, BM-derived cells may express smooth muscle actin in hypoxia-remodelled pulmonary arteries, and selective depletion of circulating BM-derived precursors prevents pulmonary adventitial remodelling, suggesting that these cells may have functional relevance in the pathophysiology of hypoxia-induced PH 3. CD117/c-kit, a transmembrane receptor tyrosine kinase for the progenitor cell factor (SCF), is a marker for BM-derived haematopoietic progenitor cells, and this receptor can be targeted by tyrosine kinase inhibitors which have been recently proposed as novel therapeutic agents to be tested in PH 4. Indeed, a novel antiproliferative-based strategy using therapeutic agents such as imatinib mesylate inhibiting several tyrosine kinases associated with disease states, including BCR-ABL, c-kit, and platelet-derived growth factor (PDGF) receptors α and β, has been demonstrated to reverse pulmonary vascular remodelling in animal models of PH (chronic hypoxia- and monocrotaline-induced PH), through inhibition of proliferation and increased apoptosis rate of pulmonary arterial smooth muscle cells 5. As imatinib has a broad spectrum of … ER -