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Young Investigator Symposium

CELL SIGNALLING AND PHENOTYPIC CHANGES IN CHRONIC HYPOXIC PULMONARY ADVENTITIAL FIBROBLASTS: POSITIVE EFFECTS OF FLUVASTASTIN ARE NOT SEEN WITH ESTABLISHED PULMONARY HYPERTENSION AGENTS
C. M. Carlin, A. J. Peacock, D. J. Welsh. Scottish Pulmonary Vascular Unit, Western Infirmary, Glasgow, UK

Background: Hypoxic pulmonary hypertension (PH) is a common and important disease. Statins partially reverse experimental PH, but so do other PH therapies and we incompletely understand their utility. In hypoxic PH, pulmonary adventitial fibroblasts (PAFs) proliferate and release mitogens, causing fibroproliferative vascular remodelling. We recently identified a Rac1–p38 MAP kinase signalling pathway as the mediator of acute hypoxia-induced proliferation in PAFs, and showed that this can be inhibited by fluvastatin (Carlin et al, AJRCMB, 2007). It is, however, unknown if statins can influence the proliferative and mitogen-releasing PAF phenotype in chronic hypoxia. To evaluate hypoxic signalling in chronic hypoxic PAFs, further assess the therapeutic potential of statins and evaluate PAF mitogen release, we studied proliferative and MAP kinase signalling in chronic hypoxic PAFs, applied conditioned media from PAFs to pulmonary artery smooth . . . [Full text of this article]