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Am. J. Respir. Cell Mol. Biol., Volume 21, Number 1, July, 1999 105-110

Autocrine Function of Inducible Nitric Oxide Synthase and Cyclooxygenase-2 in Proliferation of Human and Rat Pulmonary Artery Smooth-Muscle Cells
Species Variation

Karen B. Jourdan, Timothy W. Evans, Nick J. Lamb, Peter Goldstraw, and Jane A. Mitchell

Unit of Critical Care, Imperial College School of Medicine at the National Heart and Lung Institute, Royal Brompton Hospital, London, United Kingdom

Pulmonary hypertension is characterized by hypertrophy and hyperplasia of vascular smooth muscle occurring via an unknown mechanism. Cyclooxygenase (COX)-2 and inducible nitric oxide synthase (iNOS) are expressed under inflammatory conditions and produce mediators that regulate growth in some tissues. We have therefore addressed the question of COX-2 and iNOS involvement in proliferation of human and rat pulmonary artery (PA) smooth-muscle cells (SMC). Interleukin (IL)-1beta suppressed proliferation of both human and rat PA SMC. Moreover, IL-1beta induced COX-2 expression in both cell types. By contrast, IL-1beta stimulated the expression of iNOS protein in rat cells only. COX-2 induced in human cells inhibited proliferation, whereas COX-2 products in rat cells were without affect. However, iNOS activity in rat cells suppressed their proliferation. We conclude that human and rat evolution has diverged such that COX-2 and iNOS, although induced by the same mediator, have different levels of activity and functions in the two species. In humans, induction of COX-2 during pulmonary hypertension may be beneficial for long-term treatment of this disease.




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