Dilated bile canaliculi and attenuated decrease of nerve-dependent bile secretion in connexin32-deficient mouse liver

Research output: Contribution to journalResearch articleContributedpeer-review

Contributors

  • Achim Temme - , Institute for Immunology (Author)
  • Frank Stümpel - , University of Göttingen (Author)
  • Goran Söhl - , University of Bonn (Author)
  • Ernst Peter Rieber - , TUD Dresden University of Technology (Author)
  • Kurt Jungermann - , University of Göttingen (Author)
  • Klaus Willecke - , University of Bonn (Author)
  • Thomas Ott - , University of Bonn (Author)

Abstract

Gap junction channels in the rodent liver are composed of connexin26 (Cx26) and connexin32 (Cx32) proteins. Gap junctional intercellular communication in the mouse liver enhances the effects of hormonal or sympathetic stimulation of glucose release from glycogen stores. To determine whether contraction of bile canaliculi and bile secretion are dependent on the function of gap junction channels, we compared wild-type and connexin32-deficient mice. Confocal laser scanning microscopy of the wild-type mouse liver confirmed the close association of connexin26 and -32 proteins with the zona occludens-1 protein and actin filaments of the bile canaliculi. The decrease of bile flow after electrical stimulation of sympathetic nerves in the perfused liver was attenuated in the Cx32-deficient liver compared with wild-type controls. The amount of secreted bile, however, was similar in wild-type and Cx32-deficient livers. Furthermore, Cx32-deficient mice exhibited dilated bile canaliculi, suggesting that the contraction of bile canaliculi could be impaired in these animals.

Details

Original languageEnglish
Pages (from-to)961-966
Number of pages6
JournalPflugers Archiv European Journal of Physiology
Volume442
Issue number6
Publication statusPublished - 2001
Peer-reviewedYes

External IDs

PubMed 11680630

Keywords

Keywords

  • Bile flow, Cx26, Cx32, Gap junction, Liver