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Research Article Free access | 10.1172/JCI116998

Regulation of eicosanoid production and mitogenesis in rat intestinal epithelial cells by transforming growth factor-alpha and phorbol ester.

R N DuBois, J Awad, J Morrow, L J Roberts 2nd, and P R Bishop

Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee 37232.

Find articles by DuBois, R. in: JCI | PubMed | Google Scholar

Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee 37232.

Find articles by Awad, J. in: JCI | PubMed | Google Scholar

Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee 37232.

Find articles by Morrow, J. in: JCI | PubMed | Google Scholar

Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee 37232.

Find articles by Roberts, L. in: JCI | PubMed | Google Scholar

Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee 37232.

Find articles by Bishop, P. in: JCI | PubMed | Google Scholar

Published February 1, 1994 - More info

Published in Volume 93, Issue 2 on February 1, 1994
J Clin Invest. 1994;93(2):493–498. https://doi.org/10.1172/JCI116998.
© 1994 The American Society for Clinical Investigation
Published February 1, 1994 - Version history
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Abstract

Growth factors and tumor promoters have been shown to play a role in intestinal epithelial growth regulation and transformation. In this study, transforming growth factor-alpha (TGF alpha) and the tumor promoter, tetradecanoyl phorbol acetate (TPA), are shown to stimulate the production of eicosanoids by rat intestinal epithelial (RIE-1) cells in culture. A 4.5-kb mRNA, which hybridizes to the mouse cyclooxygenase-2 cDNA probe, is elevated 18-fold within 30 min after TGF alpha or TPA treatment. Stimulation of RIE-1 cells with TGF alpha leads to the increase of a protein (M(r) approximately 69,000), which binds a monospecific antibody to the mouse cyclooxygenase-2 protein. Dexamethasone markedly inhibits the increase of the 4.5-kb mRNA. Pretreatment of TGF alpha or TPA-stimulated RIE-1 cells with dexamethasone or cyclooxygenase inhibitors prevents the increase in eicosanoid production by these cells. Treatment of quiescent RIE-1 cells with TGF alpha stimulates mitogenesis. This mitogenic activity is blocked by pretreating the cells with dexamethasone or cyclooxygenase inhibitors. A mitogen-inducible cyclooxygenase gene is thus shown to be regulated by TGF alpha and TPA in rat intestinal epithelial cells. We suggest that products of an intestinal growth factor-inducible cyclooxygenase may play a role in the regulation of mitogenesis.

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