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Am J Physiol Gastrointest Liver Physiol (October 9, 2002). doi:10.1152/ajpgi.00226.2002
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Articles in PresS, published online ahead of print October 9, 2002
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00226.2002
Submitted on June 11, 2002
Accepted on October 2, 2002

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, Washington University, St. Louis, MO, USA
2 Division of Gastroenterology and Hepatology, University of Virginia, Charlottesville, VA, USA
3 Department of Medicine and Molecular Biology, Washington University, St. Louis, MO, USA

* To whom correspondence should be addressed. E-mail: stensnlb{at}im.wustl.edu.

The intestinal cell line I407 responds to basic fibroblast growth factor (bFGF) by up-regulating cyclooxygenase-2 (Cox-2) mRNA and protein expression and increasing prostaglandin E2 (PGE2) production. bFGF treatment of I407 cells results in phosphorylation of p38 and the p38 inhibitor SB203580 abrogates bFGF-induced PGE2 synthesis. Wild-type p38{alpha} (p38{alpha}WT) and dominant-negative p38{alpha} (p38{alpha}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 p38{alpha}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 p38{alpha}DN clones failed to up-regulate Cox-2 protein or increase PGE2 synthesis when treated with bFGF. Exogenous arachidonate did not restore PGE2 synthesis by p38{alpha}DN cells. bFGF treatment increased Cox-2 mRNA stability and the p38 inhibitor SB203580 attenuated Cox-2 mRNA stability in bFGF treated I407 cells. These data demonstrate a crucial role for p38{alpha} 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 up-regulation, since exogenous arachidonate did not restore PGE2 synthesis.




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