PMID- 9606217
OWN - NLM
STAT- MEDLINE
DCOM- 19980701
LR  - 20231213
IS  - 0021-9525 (Print)
IS  - 1540-8140 (Electronic)
IS  - 0021-9525 (Linking)
VI  - 141
IP  - 5
DP  - 1998 Jun 1
TI  - Enhanced secretion of amylase from exocrine pancreas of connexin32-deficient 
      mice.
PG  - 1267-75
AB  - 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.
FAU - Chanson, M
AU  - Chanson M
AD  - Department of Pediatrics, University of Geneva, Switzerland. 
      Marc.Chanson@hcuge.ch
FAU - Fanjul, M
AU  - Fanjul M
FAU - Bosco, D
AU  - Bosco D
FAU - Nelles, E
AU  - Nelles E
FAU - Suter, S
AU  - Suter S
FAU - Willecke, K
AU  - Willecke K
FAU - Meda, P
AU  - Meda P
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Cell Biol
JT  - The Journal of cell biology
JID - 0375356
RN  - 0 (Connexins)
RN  - EC 3.2.1.- (Amylases)
SB  - IM
MH  - Amylases/*metabolism
MH  - Animals
MH  - Cell Communication
MH  - Connexins/deficiency/genetics/*physiology
MH  - Female
MH  - Gap Junctions/metabolism/*physiology
MH  - Gene Deletion
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Pancreas/*metabolism
MH  - Gap Junction beta-1 Protein
PMC - PMC2137182
EDAT- 1998/06/12 00:00
MHDA- 1998/06/12 00:01
PMCR- 1998/12/01
CRDT- 1998/06/12 00:00
PHST- 1998/06/12 00:00 [pubmed]
PHST- 1998/06/12 00:01 [medline]
PHST- 1998/06/12 00:00 [entrez]
PHST- 1998/12/01 00:00 [pmc-release]
AID - 10.1083/jcb.141.5.1267 [doi]
PST - ppublish
SO  - J Cell Biol. 1998 Jun 1;141(5):1267-75. doi: 10.1083/jcb.141.5.1267.