FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2160037295> ?p ?o ?g. }

• W2160037295 endingPage "605" @default.
• W2160037295 startingPage "604" @default.
• W2160037295 abstract "Boucherie et al. [[1]Boucherie S, Koukoui O, Nicolas V, Combettes L. Cholestatic bile acids inhibit gap junction permeability in rat hepatocyte couplets and normal rat cholangiocytes. J Hepatol 2005;42:244–251.Google Scholar] present intriguing data showing that cholestatic, but not choleretic bile acids inhibit gap junctional intercellular communication and speculate that this inhibition might contribute to bile acid-induced cholestasis. Here, we present evidence, that gap junctional intercellular communication is not essential for the cholestatic effect of taurolithocholic acid (TLCA) and the anticholestatic effect of tauroursodeoxycholic acid (TUDCA) in the isolated perfused mouse liver. The dihydroxy bile acid, ursodeoxycholic acid, is the only efficient treatment for certain types of chronic cholestatic liver disease, yet the mechanisms of action are still under discussion [[2]Paumgartner G. Beuers U. Ursodeoxycholic acid in cholestatic liver disease: mechanisms of action and therapeutic use revisited.Hepatology. 2002; 36: 525-531Crossref PubMed Scopus (535) Google Scholar]. Experimental evidence suggests that stimulation of impaired hepatocellular secretion by calcium (Ca2+)- and protein kinase C-dependent mechanisms contributes to the anticholestatic effect of TUDCA [3Beuers U. Nathanson M.H. Isales C.M. Boyer J.L. Tauroursodeoxycholic acid stimulates hepatocellular exocytosis and mobilizes extracellular Ca++ mechanisms defective in cholestasis.J Clin Invest. 1993; 92: 2984-2993Crossref PubMed Scopus (144) Google Scholar, 4Beuers U. Bilzer M. Chittattu A. Kullak-Ublick G.A. Keppler D. Paumgartner G. et al.Tauroursodeoxycholic acid inserts the apical conjugate export pump, Mrp2, into canalicular membranes and stimulates organic anion secretion by protein kinase C-dependent mechanisms in cholestatic rat liver.Hepatology. 2001; 33: 1206-1216Crossref PubMed Scopus (216) Google Scholar]. Previous studies have emphasized the impact of gap junctional communication for the regulation of bile secretion. Hormone-mediated changes in bile flow are modulated by intercellular communication via gap junctions [[5]Nathanson M.H. Rios-Velez L. Burgstahler A.D. Mennone A. Communication via gap junctions modulates bile secretion in the isolated perfused rat liver.Gastroenterology. 1999; 116: 1176-1183Abstract Full Text Full Text PDF PubMed Scopus (66) Google Scholar]. Gap junctions also appear to be important for neurally mediated changes in hepatic bile flow, since the nerve-dependent decrease in bile flow is significantly attenuated in livers of connexin (Cx) 32-deficient mice [[6]Temme A. Stumpel F. Sohl G. Rieber E.P. Jungermann K. Willecke K. Dilated bile canaliculi and attenuated decrease of nerve-dependent bile secretion in connexin32-deficient mouse liver.Pflugers Arch. 2001; 442: 961-966Crossref PubMed Scopus (41) Google Scholar]. Because TUDCA has been observed to induce sustained increases in cytosolic free Ca2+ [[3]Beuers U. Nathanson M.H. Isales C.M. Boyer J.L. Tauroursodeoxycholic acid stimulates hepatocellular exocytosis and mobilizes extracellular Ca++ mechanisms defective in cholestasis.J Clin Invest. 1993; 92: 2984-2993Crossref PubMed Scopus (144) Google Scholar] and Ca2+ can cross hepatocyte gap junctions, we speculated that the anticholestatic effect of TUDCA may depend in part on gap junctional communication. Therefore, the effect of TUDCA on bile flow was examined in the experimental model of TLCA-induced cholestasis in isolated perfused livers of wild-type and transgenic mice lacking the Cx32 gene that encodes the major gap junction protein expressed in liver. Primary cultures of transgenic hepatocytes from these mice showed largely decreased gap junction-mediated intercellular communication, compared with wild-type hepatocytes [[7]Nelles E. Butzler C. Jung D. Temme A. Gabriel H.D. Dahl U. et al.Defective propagation of signals generated by sympathetic nerve stimulation in the liver of connexin32-deficient mice.Proc Natl Acad Sci USA. 1996; 93: 9565-9570Crossref PubMed Scopus (345) Google Scholar] and liver sections of Cx32-deficient mice showed a drastic decrease (∼96%) in the dye-spreading compared with wild-type liver [[8]Romualdi A. Niessen H. Dombrowski F. Willecke K. Ott T. Quantitative analysis of gap-junctional intercellular communication in precision-cut mouse liver slices.Cell Tissue Res. 2002; 307: 315-320Crossref PubMed Scopus (11) Google Scholar]. Isolated livers from wild-type and Cx32-deficient mice were perfused in situ for 90 min and bile flow was measured gravimetrically every 15 min [[6]Temme A. Stumpel F. Sohl G. Rieber E.P. Jungermann K. Willecke K. Dilated bile canaliculi and attenuated decrease of nerve-dependent bile secretion in connexin32-deficient mouse liver.Pflugers Arch. 2001; 442: 961-966Crossref PubMed Scopus (41) Google Scholar]. After 45 min, the bile acids TLCA and/or TUDCA, were infused for 45 min at a continuous rate into the perfusion medium to reach a final concentration of 10 μmol/L, respectively, in the portal vein. Basal bile flow was 0.97±0.38 μL/min/g liver (n=13; mean±SD) in wild-type livers and 0.69±0.13 μL/min/g liver (n=14) in Cx32-deficient livers (p<0.05). TUDCA (10 μmol/L) tended to increase bile flow by 5% in wild-type livers and by 7% in Cx32-deficient livers (n=3, each; n.s.). In contrast, TLCA (10 μmol/L) decreased bile flow by 70% in wild-type livers and by 62% in Cx32-deficient livers (n=3, each; n.s., Fig. 1). Coadministration of TUDCA counteracted TLCA-induced impairment of bile flow both in wild-type and Cx32-deficient mouse livers (79% of baseline in wild-type livers and 90% in Cx32-deficient livers, n=4, each, n.s., Fig. 1). These data indicate that the monohydroxy bile acid, TLCA, impairs bile flow and that the TLCA-induced decrease of bile flow is partially reversed by the hydrophilic bile acid, TUDCA, in wild-type and Cx32-deficient livers. These findings are in line with previous observations in perfused rat livers [[4]Beuers U. Bilzer M. Chittattu A. Kullak-Ublick G.A. Keppler D. Paumgartner G. et al.Tauroursodeoxycholic acid inserts the apical conjugate export pump, Mrp2, into canalicular membranes and stimulates organic anion secretion by protein kinase C-dependent mechanisms in cholestatic rat liver.Hepatology. 2001; 33: 1206-1216Crossref PubMed Scopus (216) Google Scholar]. The major finding of this study is, however, that these effects do not depend on gap junctional intercellular communication. Thus, these data indicate that gap junctional intercellular communication is neither essential for the cholestatic effect of TLCA nor needed for the anticholestatic effect of TUDCA in the isolated perfused mouse liver. This work was supported by grants of the German Research Association (Wi 270/24-1,2 to T.O. and K.W.) and a grant from the Förderprogramm für Forschung und Lehre der Medizinischen Fakultät der LMU München (University of Munich; to T.P.)." @default.
• W2160037295 created "2016-06-24" @default.
• W2160037295 creator A5002243456 @default.
• W2160037295 creator A5002846614 @default.
• W2160037295 creator A5018461629 @default.
• W2160037295 creator A5020192768 @default.
• W2160037295 creator A5046552100 @default.
• W2160037295 creator A5054590077 @default.
• W2160037295 date "2005-04-01" @default.
• W2160037295 modified "2023-10-15" @default.
• W2160037295 title "Gap junctional intercellular communication is not needed for the anticholestatic effect of tauroursodeoxycholic acid in mouse liver" @default.
• W2160037295 cites W1963821920 @default.
• W2160037295 cites W2008138417 @default.
• W2160037295 cites W2014105239 @default.
• W2160037295 cites W2015193975 @default.
• W2160037295 cites W2031685597 @default.
• W2160037295 cites W2048025210 @default.
• W2160037295 cites W2152680474 @default.
• W2160037295 cites W2167650510 @default.
• W2160037295 doi "https://doi.org/10.1016/j.jhep.2004.12.020" @default.
• W2160037295 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15763348" @default.
• W2160037295 hasPublicationYear "2005" @default.
• W2160037295 type Work @default.
• W2160037295 sameAs 2160037295 @default.
• W2160037295 citedByCount "3" @default.
• W2160037295 countsByYear W21600372952013 @default.
• W2160037295 countsByYear W21600372952018 @default.
• W2160037295 crossrefType "journal-article" @default.
• W2160037295 hasAuthorship W2160037295A5002243456 @default.
• W2160037295 hasAuthorship W2160037295A5002846614 @default.
• W2160037295 hasAuthorship W2160037295A5018461629 @default.
• W2160037295 hasAuthorship W2160037295A5020192768 @default.
• W2160037295 hasAuthorship W2160037295A5046552100 @default.
• W2160037295 hasAuthorship W2160037295A5054590077 @default.
• W2160037295 hasBestOaLocation W21600372951 @default.
• W2160037295 hasConcept C126322002 @default.
• W2160037295 hasConcept C134018914 @default.
• W2160037295 hasConcept C139447449 @default.
• W2160037295 hasConcept C158617107 @default.
• W2160037295 hasConcept C2777422422 @default.
• W2160037295 hasConcept C2778593092 @default.
• W2160037295 hasConcept C2779399885 @default.
• W2160037295 hasConcept C2780408053 @default.
• W2160037295 hasConcept C2780480987 @default.
• W2160037295 hasConcept C2780965833 @default.
• W2160037295 hasConcept C55493867 @default.
• W2160037295 hasConcept C71924100 @default.
• W2160037295 hasConcept C86803240 @default.
• W2160037295 hasConceptScore W2160037295C126322002 @default.
• W2160037295 hasConceptScore W2160037295C134018914 @default.
• W2160037295 hasConceptScore W2160037295C139447449 @default.
• W2160037295 hasConceptScore W2160037295C158617107 @default.
• W2160037295 hasConceptScore W2160037295C2777422422 @default.
• W2160037295 hasConceptScore W2160037295C2778593092 @default.
• W2160037295 hasConceptScore W2160037295C2779399885 @default.
• W2160037295 hasConceptScore W2160037295C2780408053 @default.
• W2160037295 hasConceptScore W2160037295C2780480987 @default.
• W2160037295 hasConceptScore W2160037295C2780965833 @default.
• W2160037295 hasConceptScore W2160037295C55493867 @default.
• W2160037295 hasConceptScore W2160037295C71924100 @default.
• W2160037295 hasConceptScore W2160037295C86803240 @default.
• W2160037295 hasIssue "4" @default.
• W2160037295 hasLocation W21600372951 @default.
• W2160037295 hasLocation W21600372952 @default.
• W2160037295 hasOpenAccess W2160037295 @default.
• W2160037295 hasPrimaryLocation W21600372951 @default.
• W2160037295 hasRelatedWork W163764920 @default.
• W2160037295 hasRelatedWork W2071036978 @default.
• W2160037295 hasRelatedWork W2087228124 @default.
• W2160037295 hasRelatedWork W2091285739 @default.
• W2160037295 hasRelatedWork W2104435845 @default.
• W2160037295 hasRelatedWork W2318835187 @default.
• W2160037295 hasRelatedWork W2341126582 @default.
• W2160037295 hasRelatedWork W2394353642 @default.
• W2160037295 hasRelatedWork W2411037392 @default.
• W2160037295 hasRelatedWork W4242180988 @default.
• W2160037295 hasVolume "42" @default.
• W2160037295 isParatext "false" @default.
• W2160037295 isRetracted "false" @default.
• W2160037295 magId "2160037295" @default.
• W2160037295 workType "article" @default.