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1, IL-1, and hypoxia on COX-2
expression in pulmonary artery smooth muscle cells
1 Division of Respiratory Medicine, University of Nottingham, City Hospital, Nottingham NG5 1PB; and 2 Thoracic Medicine, National Heart and Lung Institute, Imperial College School of Medicine, London SW3 6LY, United Kingdom
Prostanoids are
major regulators of smooth muscle function that are generated by
cyclooxygenase (COX). Here we hypothesized that cytokines and mediators
that regulate the pulmonary circulation would alter COX expression and
prostanoid generation in pulmonary artery smooth muscle cells.
Bradykinin, transforming growth factor-
1 (TGF-1), and
interleukin-1 (IL-1) increased inducible COX-2 expression and
prostaglandin E2 (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 NS-398, 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 h selectively augmented TGF-1-stimulated PGE2 production and COX-2 induction but had no effect
alone. Prolonged hypoxic culture alone for 48 and 72 h enhanced
COX-2 induction and increased PGE2. These studies show that
a number of stimuli are capable of inducing COX-2 in pulmonary artery
smooth muscle cells. The interaction between hypoxia and TGF-1 may
be particularly relevant to pulmonary hypertension.
prostaglandin E2; human; cell culture
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