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Articles in PresS, published online ahead of print May 1, 2002
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00525.2001
Submitted on December 26, 2001
Accepted on April 24, 2002
1 Department of Medicine, Veterans Affairs Center and University at Buffalo, Buffalo, NY, USA; Medicine, VA Med. Center, Buffalo, NY, USA
2 Department of Physiology & Biophysics, University at Buffalo, Buffalo, NY, USA
3 Department of Medicine, Veterans Affairs Center and University at Buffalo, Buffalo, NY, USA
4 Department of Medicine, Veterans Affairs Center and University at Buffalo, Buffalo, NY, USA; Department of Physiology & Biophysics, University at Buffalo, Buffalo, NY, USA
5 Department of Medicine, Veterans Affairs Center and University at Buffalo, Buffalo, NY, USA; Department of Physiology & Biophysics, University at Buffalo, Buffalo, NY, USA; Cancer Center, University of Arizona, Tucson, AZ, USA
* To whom correspondence should be addressed. E-mail: mplance{at}u.arizona.edu.
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 following exposure to DCA (300 µM) rose, respectively, 7-, 6- and 7-fold but CA elicited no such responses. Increases in PGE2 synthesis were preceded by sequential increases in PGH synthase-2 (PGHS-2) mRNA and protein expression, and fully prevented by a non-selective (indomethacin) or a selective (celecoxib) nonsteroidal anti-inflammatory drug (NSAID). DCA, but not CA, caused abrupt, transient increases in fibroblast [Ca2+]i approximately 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.
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