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Am J Physiol Cell Physiol 281: C188-C194, 2001;
0363-6143/01 $5.00
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Vol. 281, Issue 1, C188-C194, July 2001

COX-2 expression and cell cycle progression in human fibroblasts

Derek W. Gilroy1,2, Michael A. Saunders1, and Kenneth K. Wu1,2

1 Vascular Biology Research Center and Division of Hematology, University of Texas-Houston Medical School, Houston, Texas 77030; and 2 Institute of Biomedical Sciences, Academia Sinica, Taipei 115, Taiwan

Cyclooxygenase-2 (COX-2) is continuously expressed in most cancerous cells where it appears to modulate cellular proliferation and apoptosis. However, little is known about the contribution of transient COX-2 induction to cell cycle progression or programmed cell death in primary cells. In this study we determined whether COX-2 regulates proliferation or apoptosis in human fibroblasts. COX-2 mRNA, protein, and prostaglandin E2 (PGE2) were not detected in quiescent cells but were expressed during the G0/G1 phase of the cell cycle induced by serum. Inhibition of COX-2 did not alter G0/G1 to S phase transition or induce apoptosis at concentrations that diminished PGE2. Addition of interleukin-1beta to serum enhanced COX-2 expression and PGE2 synthesis over that by serum alone but had no effect on the progression of these cells into S phase. Furthermore, platelet-derived growth factor drove the G0 fibroblasts into the cell cycle without inducing detectable levels of COX-2 or PGE2. Collectively, these data show that transient COX-2 expression in primary human fibroblasts does not influence cell cycle progression.

serum; platelet-derived growth factor; interleukin-1beta ; proliferation; apoptosis; cyclooxygenase-2


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