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Articles in PresS, published online ahead of print March 20, 2002
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00543.2001
Submitted on December 26, 2001
Accepted on March 17, 2002
-DEPENDENT MECHANISMS
1 Department of Gastroenterology, Palo Alto Veterans Affairs Health Care System, Palo Alto, CA, USA; Department of Gastroenterology, Stanford University, Stanford, CA, USA
* To whom correspondence should be addressed. E-mail: vagt{at}leland.stanford.edu.
Barrett's esophagus (BE) results from acid and bile reflux and predisposes to adenocarcinoma. Acid and/or bile salts alter proliferation in BE in a dynamic fashion. To further understand the mechanisms of acid- and bile salt-mediated proliferation, we investigated the release of prostaglandin E2 in response to acid or bile salt exposure. Endoscopic biopsies of esophagus, BE and duodenum were exposed to a bile salt mixture (sodium glycocholate and taurocholate, glycocholic acid and deoxycholate) as a 1-h pulse and compared with exposure to pH 7.4 for up to 24 h and PGE2 release, COX-2 and PKC expression were compared. Similar experiments were also performed with acidified media (pH 3.5) alone, in the presence or absence of bisindolylmaleimide (BIM), a selective protein kinase C (PKC) inhibitor and in the presence or absence of NS-398, a cyclooxygenase-2 (COX-2) inhibitor. 1-h pulses of bile salts or acid significantly enhanced proliferation, COX-2 expression and PGE2 release in BE explants. Treatment with either BIM or NS-398 led to a dramatic decrease in PGE2 release in BE explants, and a suppression of proliferation. The acid- or bile salt-mediated hyperproliferation is related to PGE2 release. Acid- and bile salt-induced induction of COX-2 and PKC may explain, at least in part, the tumor-promoting effects of acid and bile salts in BE.
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