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Am J Physiol Gastrointest Liver Physiol 284: G205-G212, 2003. First published November 6, 2002; doi:10.1152/ajpgi.00292.2002
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Vol. 284, Issue 2, G205-G212, February 2003

Bile salts potentiate adenylyl cyclase activity and cAMP-regulated secretion in human gallbladder epithelium

Nicolas Chignard1, Martine Mergey1, Danielle Veissière1, Raoul Poupon1,2, Jacqueline Capeau1,3, Rolland Parc4, Annick Paul1, and Chantal Housset 1,2,3

1 Institut National de la Santé et de la Recherche Médicale, 2 Service d'Hépatologie, Hôpital Saint-Antoine, and 4 Service de Chirurgie Générale et Digestive, Hôpital Saint-Antoine, 75012 Paris; and 3 Service de Biochimie, Hôpital Tenon, 75020 Paris, France

Fluid and ion secretion in the gallbladder is mainly triggered by the intracellular second messenger cAMP. We examined the action of bile salts on the cAMP-dependent pathway in the gallbladder epithelium. Primary cultures of human gallbladder epithelial cells were exposed to agonists of the cAMP pathway and/or to bile salts. Taurochenodeoxycholate and tauroursodeoxycholate increased forskolin-induced cAMP accumulation to a similar extent, without affecting cAMP basal levels. This potentiating effect was abrogated after PKC inhibition, whereas both taurochenodeoxycholate and tauroursodeoxycholate induced PKC-alpha and -delta translocation to cell membranes. Consistent with a PKC-mediated stimulation of cAMP production, the expression of six adenylyl cyclase isoforms, including PKC-regulated isoforms 5 and 7, was identified in human gallbladder epithelial cells. cAMP-dependent chloride secretion induced by isoproterenol, a beta -adrenergic agonist, was significantly increased by taurochenodeoxycholate and by tauroursodeoxycholate. In conclusion, endogenous and therapeutic bile salts via PKC regulation of adenylyl cyclase activity potentiate cAMP production in the human gallbladder epithelium. Through this action, bile salts may increase fluid secretion in the gallbladder after feeding.

beta -adrenergic agonist; chenodeoxycholic acid; chloride channels; ursodeoxycholic acid


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