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Articles in PresS, published online ahead of print May 10, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00070.2002
Submitted on February 28, 2002
Accepted on April 25, 2002
1 Division of Respiratory Medicine, University of Nottingham, Nottingham, Notts, United Kingdom
2 Thoracic Medicine, Imperial College School of Medicine, London, London, United Kingdom
* To whom correspondence should be addressed. E-mail: dawn.bradbury{at}nottingham.ac.uk.
Prostanoids are major regulators of smooth muscle function which are generated by cyclooxygenase (COX). Here we hypothesised that cytokines and mediators which regulate the pulmonary circulation would alter COX expression and prostanoid generation in pulmonary artery smooth muscle cells (PASMC). Bradykinin, TGF-ß1 and IL-1ß increased inducible COX-2 expression and PGE2 release. Transfection studies using a COX-2 promoter construct demonstrated that all three agents acted transcriptionally. Constitutive COX-1 protein expression was unchanged. The COX inhibitor indomethacin, the COX-2 inhibitor NS398, the protein synthesis inhibitor cycloheximide and the glucocorticoid dexamethasone abrogated the increased PGE2 levels. Dexamethasone and cycloheximide prevented COX-2 induction. Hypoxia (3% O2/5% CO2/92% N2) for 24 hours selectively augmented TGF-ß1 stimulated PGE2 production and COX-2 induction but had no effect alone. Prolonged hypoxic culture for 48 and 72 hours enhanced COX-2 induction and increased PGE2 on its own. These studies show that a number of stimuli are capable of inducing COX-2 in PASMC. The interaction between hypoxia and TGF-ß1 may be particularly relevant to pulmonary hypertension.
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