ArticleThe Journal of clinical investigation1999
Defective regulation of gap junctional coupling in cystic fibrosis pancreatic duct cells.
Article in The Journal of clinical investigation, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 47 citations in OpenAlex.
- Functional Rescue of CFTR-Dependent Transport in a Pancreatic Ductal Epithelial Cell Model: The Impact of Pharmacological Modulation and Inflammation.International journal of molecular sciences · 2026Article
- Article
- Defective goblet cell exocytosis contributes to murine cystic fibrosis-associated intestinal disease.The Journal of clinical investigation · 2015Article
- Effect of polarized release of CXC-chemokines from wild-type and cystic fibrosis murine airway epithelial cells.American journal of respiratory cell and molecular biology · 2011Article
- Prostaglandin E₂regulation of cystic fibrosis transmembrane conductance regulator activity and airway surface liquid volume requires gap junctional communication.American journal of respiratory cell and molecular biology · 2011Article
- Cystic fibrosis transmembrane conductance regulator trafficking modulates the barrier function of airway epithelial cell monolayers.The Journal of physiology · 2010Article
- Pass the bicarb: the importance of HCO3- for mucin release.The Journal of clinical investigation · 2009Article
- Interplay between cystic fibrosis transmembrane regulator and gap junction channels made of connexins 45, 40, 32 and 50 expressed in oocytes.The Journal of membrane biology · 2006Article
- The hormonal control of uterine luminal fluid secretion and absorption.The Journal of membrane biology · 2005Article
- Functional interaction between CFTR and Cx45 gap junction channels expressed in oocytes.The Journal of membrane biology · 2005Article
- Regulation of gap junctional communication by a pro-inflammatory cytokine in cystic fibrosis transmembrane conductance regulator-expressing but not cystic fibrosis airway cells.The American journal of pathology · 2001Article
- Cystic fibrosis transmembrane conductance regulator does not affect neutrophil migration across cystic fibrosis airway epithelial monolayers.The American journal of pathology · 2000Article
- Interactions of connexins with other membrane channels and transporters.Progress in biophysics and molecular biologyReview
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cystic fibrosis (CF) gene encodes a cAMP-gated Cl- channel (cystic fibrosis transmembrane conductance regulator [CFTR]) that mediates fluid transport across the luminal surfaces of a variety of epithelial cells. We have previously shown that gap junctional communication and Cl- secretion were concurrently regulated by cAMP in cells expressing CFTR. To determine whether intercellular communication and CFTR-dependent secretion are related, we have compared gap junctional coupling in a human pancreatic cell line harboring the DeltaF508 mutation in CFTR and in the same cell line in which the defect was corrected by transfection with wild-type CFTR. Both cell lines expressed connexin45 (Cx45), as evidenced by RT-PCR, immunocytochemistry, and dual patch-clamp recording. Exposure to agents that elevate intracellular cAMP or specifically activate protein kinase A evoked Cl- currents and markedly increased junctional conductance of CFTR-expressing pairs, but not in the parental cells. The latter effect, which was caused by an increase in single-channel activity but not in unitary conductance of Cx45 channels, was not prevented by exposing CFTR-expressing cells to a Cl- channel blocker. We conclude that expression of functional CFTR restored the cAMP-dependent regulation of junctional conductance in CF cells. Direct intercellular communication coordinates multicellular activity in tissues that are major targets of CF manifestations. Consequently, defective regulation of gap junction channels may contribute to the altered functions of tissues affected in CF.
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