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.
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1 June 1998
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June 01 1998
Enhanced Secretion of Amylase from Exocrine Pancreas of Connexin32-deficient Mice
Marc Chanson,
Marc Chanson
*Department of Pediatrics, ‡Department of Morphology, University of Geneva, Switzerland; §Laboratory of Cell Biology, University Paul Sabatier, France; and ‖Institute for Genetics, University of Bonn, Germany
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Marjorie Fanjul,
Marjorie Fanjul
*Department of Pediatrics, ‡Department of Morphology, University of Geneva, Switzerland; §Laboratory of Cell Biology, University Paul Sabatier, France; and ‖Institute for Genetics, University of Bonn, Germany
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Domenico Bosco,
Domenico Bosco
*Department of Pediatrics, ‡Department of Morphology, University of Geneva, Switzerland; §Laboratory of Cell Biology, University Paul Sabatier, France; and ‖Institute for Genetics, University of Bonn, Germany
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Eric Nelles,
Eric Nelles
*Department of Pediatrics, ‡Department of Morphology, University of Geneva, Switzerland; §Laboratory of Cell Biology, University Paul Sabatier, France; and ‖Institute for Genetics, University of Bonn, Germany
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Susanne Suter,
Susanne Suter
*Department of Pediatrics, ‡Department of Morphology, University of Geneva, Switzerland; §Laboratory of Cell Biology, University Paul Sabatier, France; and ‖Institute for Genetics, University of Bonn, Germany
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Klaus Willecke,
Klaus Willecke
*Department of Pediatrics, ‡Department of Morphology, University of Geneva, Switzerland; §Laboratory of Cell Biology, University Paul Sabatier, France; and ‖Institute for Genetics, University of Bonn, Germany
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Paolo Meda
Paolo Meda
*Department of Pediatrics, ‡Department of Morphology, University of Geneva, Switzerland; §Laboratory of Cell Biology, University Paul Sabatier, France; and ‖Institute for Genetics, University of Bonn, Germany
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Marc Chanson
*Department of Pediatrics, ‡Department of Morphology, University of Geneva, Switzerland; §Laboratory of Cell Biology, University Paul Sabatier, France; and ‖Institute for Genetics, University of Bonn, Germany
Marjorie Fanjul
*Department of Pediatrics, ‡Department of Morphology, University of Geneva, Switzerland; §Laboratory of Cell Biology, University Paul Sabatier, France; and ‖Institute for Genetics, University of Bonn, Germany
Domenico Bosco
*Department of Pediatrics, ‡Department of Morphology, University of Geneva, Switzerland; §Laboratory of Cell Biology, University Paul Sabatier, France; and ‖Institute for Genetics, University of Bonn, Germany
Eric Nelles
*Department of Pediatrics, ‡Department of Morphology, University of Geneva, Switzerland; §Laboratory of Cell Biology, University Paul Sabatier, France; and ‖Institute for Genetics, University of Bonn, Germany
Susanne Suter
*Department of Pediatrics, ‡Department of Morphology, University of Geneva, Switzerland; §Laboratory of Cell Biology, University Paul Sabatier, France; and ‖Institute for Genetics, University of Bonn, Germany
Klaus Willecke
*Department of Pediatrics, ‡Department of Morphology, University of Geneva, Switzerland; §Laboratory of Cell Biology, University Paul Sabatier, France; and ‖Institute for Genetics, University of Bonn, Germany
Paolo Meda
*Department of Pediatrics, ‡Department of Morphology, University of Geneva, Switzerland; §Laboratory of Cell Biology, University Paul Sabatier, France; and ‖Institute for Genetics, University of Bonn, Germany
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: [email protected]
Received:
December 29 1997
Revision Received:
April 29 1998
Online ISSN: 1540-8140
Print ISSN: 0021-9525
1998
J Cell Biol (1998) 141 (5): 1267–1275.
Article history
Received:
December 29 1997
Revision Received:
April 29 1998
Citation
Marc Chanson, Marjorie Fanjul, Domenico Bosco, Eric Nelles, Susanne Suter, Klaus Willecke, Paolo Meda; Enhanced Secretion of Amylase from Exocrine Pancreas of Connexin32-deficient Mice . J Cell Biol 1 June 1998; 141 (5): 1267–1275. doi: https://doi.org/10.1083/jcb.141.5.1267
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