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Related Experiment Videos

Rabbit pancreatic acini express CFTR as a cAMP-activated chloride efflux pathway

H Kopelman1, E Ferretti, C Gauthier

  • 1Department of Pediatrics, McGill University-Montreal Children's Hospital Research Institute, Quebec, Canada.

The American Journal of Physiology
|September 1, 1995
PubMed
Summary

Cystic fibrosis transmembrane conductance regulator (CFTR) is expressed in rabbit pancreatic acini. CFTR antisense oligodeoxynucleotide selectively inhibited cAMP-activated chloride efflux, confirming its role in acinar cells.

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Physiology

Background:

  • Epithelial cells utilize Cystic fibrosis transmembrane conductance regulator (CFTR) for cAMP-activated chloride transport.
  • Rabbit pancreatic acini exhibit cAMP-activated chloride efflux independent of zymogen granule secretion.

Purpose of the Study:

  • To investigate the presence and function of CFTR in isolated rabbit pancreatic acini.
  • To determine if CFTR mediates the cAMP-activated chloride efflux in these cells.

Main Methods:

  • Polymerase chain reaction (PCR) was used to amplify a CFTR sequence from acinar RNA.
  • Western blotting with a CFTR antibody (M3A7) identified CFTR protein in acinar membranes.
  • CFTR antisense oligodeoxynucleotide was used to inhibit chloride efflux in acinar cells.

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Main Results:

  • A 480-bp PCR product homologous to human CFTR was amplified from acinar RNA.
  • CFTR antibody recognized 180- and 160-kDa proteins in acinar membranes.
  • CFTR antisense treatment selectively inhibited cAMP-activated chloride efflux without affecting amylase secretion.

Conclusions:

  • These findings confirm the expression of CFTR in rabbit pancreatic acini.
  • CFTR is responsible for cAMP-activated chloride efflux in pancreatic acini.
  • Isolated pancreatic acini are a suitable model for studying CFTR function.