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Am J Physiol Gastrointest Liver Physiol 284: G269-G279, 2003. First published October 9, 2002; doi:10.1152/ajpgi.00226.2002
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Vol. 284, Issue 2, G269-G279, February 2003

Basic fibroblast growth factor upregulates cyclooxygenase-2 in I407 cells through p38 MAP kinase

Teresa G. Tessner1, Filipe Muhale1, Suzanne Schloemann1, Steven M. Cohn2, Aubrey Morrison3, and William F. Stenson1

1 Division of Gastroenterology, 3 Department of Medicine and Molecular Biology and Pharmacology, Washington University, St. Louis, Missouri 63110; and 2 Division of Gastroenterology and Hepatology, University of Virginia, Charlottesville, Virginia 22904

The intestinal cell line I407 responds to basic fibroblast growth factor (bFGF) by upregulating cyclooxygenase-2 (COX-2) mRNA and protein expression and increasing PGE2 production. bFGF treatment of I407 cells results in phosphorylation of p38, and the p38 inhibitor SB-203580 abrogates bFGF-induced PGE2 synthesis. Wild-type p38alpha (p38alpha WT) and dominant-negative p38alpha (p38alpha DN) stable transfectant clones of I407 cells were used to examine the role of the p38 MAP kinase pathway in the events controlling PGE2 synthesis after treatment with bFGF. Treatment of p38alpha WT clones with bFGF resulted in increased COX-2 protein levels and PGE2 synthesis similar to those seen in bFGF-treated control-transfected cells. In contrast, the p38alpha DN clones failed to upregulate COX-2 protein or increase PGE2 synthesis when treated with bFGF. Exogenous arachidonate did not restore PGE2 synthesis by p38alpha DN cells. bFGF treatment increased COX-2 mRNA stability, and the p38 inhibitor SB-203580 attenuated COX-2 mRNA stability in bFGF-treated I407 cells. These data demonstrate a crucial role for p38alpha in growth factor-induced PGE2 synthesis by intestinal cells. Furthermore, they indicate that p38 activity is required at a step distal to arachidonate release, most likely COX-2 upregulation, because exogenous arachidonate did not restore PGE2 synthesis.

intestinal epithelial cells; intestinal injury and repair; arachidonic acid metabolism; mRNA stability.


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