JCB logo
BITPLANE Scientific Software
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents

This Article
Right arrow Full Text
Right arrow Full Text (PDF, 664K)
Right arrow PPT slides of all figures
Right arrow Alert me when this article is cited
Right arrow Citation Map
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new content in the JCB
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Chanson, M.
Right arrow Articles by Meda, P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Chanson, M.
Right arrow Articles by Meda, P.
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Facebook   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?

© The Rockefeller University Press, 0021-9525/1998//1267 $5.00
The Journal of Cell Biology, Volume 141, Number 5, , 1998 1267-1275


Articles

Enhanced Secretion of Amylase from Exocrine Pancreas of Connexin32-deficient Mice



Marc Chanson*, Marjorie Fanjul§, Domenico Bosco{ddagger}, Eric Nelles||, Susanne Suter*, Klaus Willecke||, and Paolo Meda{ddagger}

* Department of Pediatrics, {ddagger} Department of Morphology, University of Geneva, Switzerland; § Laboratory of Cell Biology, University Paul Sabatier, France; and || Institute for Genetics, University of Bonn, Germany

To determine whether junctional communication between pancreatic acinar cells contributes to their secretory function in vivo, we have compared wild-type mice, which express the gap junctional proteins connexin32 (Cx32) and connexin26, to mice deficient for the Cx32 gene. Pancreatic acinar cells from Cx32 (–/–) mice failed to express Cx32 as evidenced by reverse transcription–PCR and immunolabeling and showed a marked reduction (4.8- and 25-fold, respectively) in the number and size of gap junctions. Dye transfer studies showed that the extent of intercellular communication was inhibited in Cx32 (–/–) acini. However, electrical coupling was detected by dual patch clamp recording in Cx32 (–/–) acinar cell pairs. Although wild-type and Cx32 (–/–) acini were similarly stimulated to release amylase by carbamylcholine, Cx32 (–/–) acini showed a twofold increase of their basal secretion. This effect was caused by an increase in the proportion of secreting acini, as detected with a reverse hemolytic plaque assay. Blood measurements further revealed that Cx32 (–/–) mice had elevated basal levels of circulating amylase. The results, which demonstrate an inverse relationship between the extent of acinar cell coupling and basal amylase secretion in vivo, support the view that the physiological recruitment of secretory acinar cells is regulated by gap junction mediated intercellular communication.


Abbreviations used in this paper: CCH, carbamylcholine; Cx, connexin; RT, reverse transcription.

Address all correspondence to Marc Chanson, Laboratory of Clinical Investigation 3, HUG, Department of Pediatrics, P.O. Box 14, 24 Micheli-du-Crest, 1211 Geneva 4, Switzerland. Tel.: (41 22) 37 24 609. Fax: (41 22) 37 24 088. E-mail: Marc.Chanson{at}hcuge.ch



Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Facebook Facebook   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter    What's this?


This article has been cited by other articles:



  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents