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Am J Physiol Gastrointest Liver Physiol 283: G503-G510, 2002. First published May 1, 2002; doi:10.1152/ajpgi.00525.2001
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Vol. 283, Issue 3, G503-G510, September 2002

TRANSLATIONAL PHYSIOLOGY
Ca2+- and PKC-dependent stimulation of PGE2 synthesis by deoxycholic acid in human colonic fibroblasts

Yingting Zhu1, Ping Hua2, Shazia Rafiq1, Eric J. Waffner1, Michael E. Duffey1,2, and Peter Lance1,2

1 Department of Medicine, Veterans Affairs Medical Center and 2 Department of Physiology and Biophysics, University at Buffalo, Buffalo, New York 14215

We investigated prostanoid biogenesis by human colonic fibroblasts (CCD-18Co cells and nine primary fibroblast cultures) exposed to a primary (cholic, CA) or a secondary (deoxycholic, DCA) bile acid. Basal PGE2 levels in CCD-18Co cultures and fibroblast strains initiated from normal and adenocarcinomatous colon, respectively, were 1.7 ± 0.3, 4.0 ± 2.0, and 15.0 ± 4.8 ng/mg protein. Peak levels 24 h after exposure to DCA (300 µM) rose, respectively, seven-, six- and sevenfold, but CA elicited no such responses. Increases in PGE2 synthesis were preceded by sequential increases in PGH synthase-2 mRNA and protein expression and were fully prevented by a nonselective (indomethacin) or a selective (celecoxib) nonsteroidal anti-inflammatory drug. DCA, but not CA, caused abrupt, transient increases in fibroblast intracellular Ca2+ concentration ([Ca2+]i) ~1 min after exposure. Increased [Ca2+]i was required for DCA-mediated induction of PGE2 synthesis, and protein kinase C was a further essential component of this signaling pathway. Colonic fibroblasts may be a major target for prostanoid biogenesis induced by fecal bile acids and, potentially, other noxious actions of these agents.

colorectal neoplasms; feces; mesenchymal cells; prostaglandin H synthases


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