Stimulation of bile acid active transport related to increased mucosal cyclic AMP content in rat ileum in vitro

Reymann, Andreas; Braun, W.; Drobik, Christian; Woermann, Cornelia

doi:10.1016/0167-4889(89)90203-6

Cited by 19 publications

(10 citation statements)

References 36 publications

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“…NTCP and ASBT are expressed in various cell types such as hepatocytes, intestinal enterocytes, renal proximal tubular cells and function to maintain the enterohepatic circulation of bile acids in the body (Dawson et al, 2009; Trauner and Boyer, 2003). These bile acid transporters reside on the cell plasma membrane and recycle back to the cell surface once internalized (Alpini et al, 2005; Grune et al, 1993; Mukhopadhayay et al, 1997; Reymann et al, 1989). Previously, our group reported that PKA signaling pathway is important in bile- or IC-mediated PEC replication (Chang et al, 2002; Chang et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

“…Previously, our group reported that PKA signaling pathway is important in bile- or IC-mediated PEC replication (Chang et al, 2002; Chang et al, 2004). Since recycling of bile acid transporters is regulated by cAMP-dependent PKA pathway (Alpini et al, 2005; Grune et al, 1993; Mukhopadhayay et al, 1997; Reymann et al, 1989), it seems plausible that the importance of cAMP-dependent PKA pathway in bile acid-mediated PEC replication stems from its involvement in recycling of bile acid transporters in the cells. However, further study is required to clarify the roles of PKA pathway in bile acid-supported PEC replication.…”

Section: Discussionmentioning

confidence: 99%

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The crucial role of bile acids in the entry of porcine enteric calicivirus

2014

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Replication of porcine enteric calicivirus (PEC) in LLC-PK cells is dependent on the presence of bile acids in the medium. However, the mechanism of bile acid-dependent PEC replication is unknown. Understanding of bile acid-mediated PEC replication may provide insight into cultivating related human noroviruses, currently uncultivable, which are the major cause of viral gastroenteritis outbreaks in humans. Our results demonstrated that while uptake of PEC into the endosomes does not require bile acids, the presence of bile acids is critical for viral escape from the endosomes into cell cytoplasm to initiate viral replication. We also demonstrated that bile acid transporters including the sodium-taurocholate co-transporting polypeptide and the apical sodium-dependent bile acid transporter are important in exerting the effects of bile acids in PEC replication in cells. In summary, our results suggest that bile acids play a critical role in virus entry for successful replication.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

The crucial role of bile acids in the entry of porcine enteric calicivirus

2014

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“…Cyclic AMP-dependent increases in apical ASBT in rat cholangiocytes (3) and rat ileum (128) have been reported. Secretin, acting via cAMP, increases apical ASBT in rat cholangiocytes, which is reversible and requires intact microtubules (3).…”

Section: Post-translational Regulation Of Ntcp and Asbtmentioning

confidence: 98%

Sodium-dependent bile salt transporters of the SLC10A transporter family: more than solute transporters

Anwer

Stieger

2013

Pflugers Arch - Eur J Physiol

129

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Summary The SLC10A transporter gene family consists of seven members and substrates transported by three members (SLC10A1, SLC10A2 and SLC10A6) are Na+-dependent. SLC10A1 (sodium taurocholate cotransporting polypeptide or NTCP) and SLC10A2 (apical sodium-dependent bile salt transporter or ASBT) transport bile salts and play an important role in maintaining enterohepatic circulation of bile salts. Solutes other than bile salts are also transported by NTCP. However, ASBT has not been shown to be a transporter for non-bile salt substrates. While the transport function of NTCP can potentially be used as liver function test, interpretation of such a test may be complicated by altered expression of NTCP in diseases and presence of drugs that may inhibit NTCP function. Transport of bile salts by NTCP and ASBT is inhibited by a number of drugs and it appears that ASBT is more permissive to drug inhibition than NTCP. The clinical significance of this inhibition in drug disposition and drug-drug interaction remains to be determined. Both NCTP and ASBT undergo post-translational regulations that involve phosphorylation/dephosphorylation, translocation to and retrieval from the plasma membrane and degradation by the ubiquitin-proteasome system. These posttranslational regulations are mediated via signaling pathways involving cAMP, calcium, nitric oxide, phosphoinositide-3-kinase (PI3K), protein kinase C (PKC) and protein phosphatases. There appears to be species difference in the substrate specificity and the regulation of plasma membrane localization of human and rodent NTCP. These differences should be taken into account when extrapolating rodent data for human clinical relevance and developing novel therapies. NTCP has recently been shown to play an important role in HBV and HDV infection by serving as a receptor for entry of these viruses into hepatocytes.

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“…1,13 Identical with our findings in cholangiocytes, increased intracellular cAMP stimulates ASBT activity in the ileum. 22 Cholehepatic Shunting. Bile acid secretion at the hepatocyte canalicular membrane occurs because of the presence of facilitated and active transport.…”

Section: Discussionmentioning

confidence: 99%

Secretin activation of the apical Na+‐dependent bile acid transporter is associated with cholehepatic shunting in rats†

et al. 2005

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The role of the cholangiocyte apical Na ؉ -dependent bile acid transporter (ASBT) in bile formation is unknown. Bile acid absorption by bile ducts results in cholehepatic shunting, a pathway that amplifies the canalicular osmotic effects of bile acids. We tested in isolated cholangiocytes if secretin enhances ASBT translocation to the apical membrane from latent preexisting intracellular stores. In vivo, in bile duct-ligated rats, we tested if increased ASBT activity (induced by secretin pretreatment) results in cholehepatic shunting of bile acids. We determined the increment in taurocholate-dependent bile flow and biliary lipid secretion and taurocholate (TC) biliary transit time during high ASBT activity. Secretin stimulated colchicine-sensitive ASBT translocation to the cholangiocyte plasma membrane and 3 H-TC uptake in purified cholangiocytes. Consistent with increased ASBT promoting cholehepatic shunting, with secretin pretreatment, we found TC induced greater-than-expected biliary lipid secretion and bile flow and there was a prolongation of the TC biliary transit time.

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Stimulation of bile acid active transport related to increased mucosal cyclic AMP content in rat ileum in vitro

Cited by 19 publications

References 36 publications

The crucial role of bile acids in the entry of porcine enteric calicivirus

The crucial role of bile acids in the entry of porcine enteric calicivirus

Sodium-dependent bile salt transporters of the SLC10A transporter family: more than solute transporters

Secretin activation of the apical Na+‐dependent bile acid transporter is associated with cholehepatic shunting in rats†

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