Stimulation of HCO3– Secretion across Cystic Fibrosis Pancreatic Duct Cells by Extracellular ATP

Neurosignals ◽  
1998 ◽  
Vol 7 (6) ◽  
pp. 321-327 ◽  
Author(s):  
C.Y. Cheung ◽  
X.F. Wang ◽  
H.C. Chan
Keyword(s):  
Cystic Fibrosis ◽  
Pancreatic Duct ◽  
Extracellular Atp ◽  
Duct Cells ◽  
Pancreatic Duct Cells ◽  
Stimulation Of

CFTR gene transfer to human cystic fibrosis pancreatic duct cells using a Sendai virus vector

2007 ◽  
Vol 214 (2) ◽  
pp. 442-455 ◽  
Author(s):  
Zoltán Rakonczay ◽  
Péter Hegyi ◽  
Mamoru Hasegawa ◽  
Makoto Inoue ◽  
Jun You ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Gene Transfer ◽  
Pancreatic Duct ◽  
Sendai Virus ◽  
Virus Vector ◽  
Cftr Gene ◽  
Duct Cells ◽  
Pancreatic Duct Cells

scholarly journals CFTR Functions as a Bicarbonate Channel in Pancreatic Duct Cells

2009 ◽  
Vol 133 (3) ◽  
pp. 315-326 ◽  
Author(s):  
Hiroshi Ishiguro ◽  
Martin C. Steward ◽  
Satoru Naruse ◽  
Shigeru B.H. Ko ◽  
Hidemi Goto ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Membrane Potential ◽  
Guinea Pig ◽  
Pancreatic Duct ◽  
Apical Membrane ◽  
Transmembrane Conductance Regulator ◽  
Duct Cells ◽  
Pancreatic Duct Cells ◽  
K Concentration ◽  
Significant Pathway

Pancreatic duct epithelium secretes a HCO3−-rich fluid by a mechanism dependent on cystic fibrosis transmembrane conductance regulator (CFTR) in the apical membrane. However, the exact role of CFTR remains unclear. One possibility is that the HCO3− permeability of CFTR provides a pathway for apical HCO3− efflux during maximal secretion. We have therefore attempted to measure electrodiffusive fluxes of HCO3− induced by changes in membrane potential across the apical membrane of interlobular ducts isolated from the guinea pig pancreas. This was done by recording the changes in intracellular pH (pHi) that occurred in luminally perfused ducts when membrane potential was altered by manipulation of bath K+ concentration. Apical HCO3− fluxes activated by cyclic AMP were independent of Cl− and luminal Na+, and substantially inhibited by the CFTR blocker, CFTRinh-172. Furthermore, comparable HCO3− fluxes observed in ducts isolated from wild-type mice were absent in ducts from cystic fibrosis (ΔF) mice. To estimate the HCO3− permeability of the apical membrane under physiological conditions, guinea pig ducts were luminally perfused with a solution containing 125 mM HCO3− and 24 mM Cl− in the presence of 5% CO2. From the changes in pHi, membrane potential, and buffering capacity, the flux and electrochemical gradient of HCO3− across the apical membrane were determined and used to calculate the HCO3− permeability. Our estimate of ∼0.1 µm sec−1 for the apical HCO3− permeability of guinea pig duct cells under these conditions is close to the value required to account for observed rates of HCO3− secretion. This suggests that CFTR functions as a HCO3− channel in pancreatic duct cells, and that it provides a significant pathway for HCO3− transport across the apical membrane.

CFTR and calcium-activated chloride currents in pancreatic duct cells of a transgenic CF mouse

1994 ◽  
Vol 266 (1) ◽  
pp. C213-C221 ◽  
Author(s):  
M. A. Gray ◽  
J. P. Winpenny ◽  
D. J. Porteous ◽  
J. R. Dorin ◽  
B. E. Argent
Keyword(s):  
Cystic Fibrosis ◽  
Pancreatic Duct ◽  
Chloride Channels ◽  
Insertional Mutagenesis ◽  
Secretory Pathway ◽  
Exon Skipping ◽  
Wild Type ◽  
Chloride Currents ◽  
Duct Cells ◽  
Pancreatic Duct Cells

We have studied the cystic fibrosis transmembrane conductance regulator (CFTR) and calcium-activated chloride currents in pancreatic duct cells isolated from a transgenic cf/cf mouse created by targeted insertional mutagenesis. Adenosine 3',5'-cyclic monophosphate (cAMP)-activated CFTR chloride currents were detected in 78% (29/37) of wild-type cells, in 81% (35/43) of heterozygote cells, and in 61% (29/47) of homozygous cf/cf duct cells (P > 0.05, cf/cf vs. wild-type and heterozygote). The CFTR current density measured at membrane potentials of +/- 60 mV averaged 22-26 pA/pF in wild-type and heterozygote groups but only 13 pA/pF in cells derived from cf/cf animals (P < 0.05, cf/cf vs. wild-type and cf/cf vs. heterozygotes). In contrast, duct cells from animals of all three genotypic groups exhibited calcium-activated chloride currents that were of similar magnitude and up to 11-fold larger than the CFTR currents. We speculate that these transgenic insertional null mice do not develop the pancreatic pathology that occurs in cystic fibrosis patients because their duct cells contain 1) some wild-type CFTR generated by exon skipping and aberrant splicing and 2) a separate anion secretory pathway mediated by calcium-activated chloride channels.

Stimulation of DNA Synthesis in Pancreatic Duct Cells by Gastrointestinal Hormones

Pancreas ◽  
1992 ◽  
Vol 7 (3) ◽  
pp. 271-279 ◽  
Author(s):  
Mario M. Mangino ◽  
Susan Hubchak ◽  
Dante G. Scarpelli
Keyword(s):  
Dna Synthesis ◽  
Pancreatic Duct ◽  
Gastrointestinal Hormones ◽  
Duct Cells ◽  
Pancreatic Duct Cells ◽  
Stimulation Of
Sign in / Sign up

Export Citation Format

Share Document