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Am J Physiol Cell Physiol 276: C848-C855, 1999;
0363-6143/99 $5.00
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Vol. 276, Issue 4, C848-C855, April 1999

TGF-alpha reduces bradykinin-stimulated ion transport and prostaglandin release in human colonic epithelial cells

J. Beltinger, C. J. Hawkey, and W. A. Stack

Division of Gastroenterology, University Hospital, University of Nottingham, Nottingham NG7 2UH, United Kingdom

The effect of chronic exposure to transforming growth factor-alpha (TGF-alpha ) on bradykinin-stimulated acute prostanoid production and ion secretion in monolayers of HCA-7 colony 29 colonic epithelial cells has been studied. Monolayers synthesized prostaglandin E2 (PGE2) at a basal rate of 2.10 ± 0.31 pg · monolayer-1 · min-1 over 24 h. Bradykinin (10-8-10-5 M) dose dependently increased acute PGE2 release by three orders of magnitude. This was associated with a rise in cAMP from 1.60 ± 0.14 to 2.90 ± 0.1 pmol/monolayer (P < 0.02) and a dose-dependent increase in short-circuit current (SCC). When monolayers were primed by a 24-h exposure to TGF-alpha , basal PGE2 release rose to 6.31 ± 0.38 pg · monolayer-1 · min-1 (TGF-alpha concn 10 ng/ml; P = 0.001). However, the stimulation of acute prostaglandin release, intracellular cAMP, and increased SCC by bradykinin was significantly reduced by preincubation with TGF-alpha . Priming with PGE2 (10-8-10-6 M) over 24 h mimicked the effect of TGF-alpha on bradykinin-induced changes in cAMP and SCC. These data suggest that enhanced chronic release of prostaglandins in response to stimulation with TGF-alpha may downregulate acute responses to bradykinin. In vivo, TGF-alpha could have an important modulatory function in regulating secretion under inflammatory conditions.

transforming growth factor-alpha ; cyclooxygenase; electrogenic ion transport


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