Cystic Fibrosis Research Today is a free monthly online journal that collates and summarizes the latest research about Cystic Fibrosis, including details on symptoms, genetics, treatment, information.

Chronic exposure to EGF affects trafficking and function of ENaC channel in cystic fibrosis cells.

Cao L, Owsianik G, Becq F, Nilius B

Department of Physiology, KU Leuven, Campus Gasthuisberg, Herestraat 49, B-3000 Leuven, Belgium.

Using the whole-cell patch-clamp technique, we identified an amiloride (AMI)-sensitive Na(+) current in cystic fibrosis cells, JME/CF15, growing in standard medium. The reversal potential of this current depended on Na(+) concentrations and the cation selectivity was much higher for Na(+) than for K(+), indicating that the current is through ENaC channels. In contrast, cells from EGF-containing medium lacked AMI-sensitive Na(+) currents. In permeabilized cells growing in EGF-containing medium, alphaENaC was mainly detected in a perinuclear region, while in cells from standard medium it was distributed over the cell body. Western-blot analysis showed that in standard medium cells expressed fast-migrating EndoH-insensitive and slow-migrating EndoH-sensitive alphaENaC fractions, while in cells growing in the presence of EGF, alphaENaC was only detected as the fast-migrating EndoH-insensitive fraction. Long-term incubation of cells with EGF resulted in an increased basal Ca(2+) level, [Ca(2+)](i). A similar increase of [Ca(2+)](i) was also observed in the presence of 2muM thapsigargin, resulting in inhibition of ENaC function. Thus, in JME/CF15 cells inhibition of the ENaC function by chronic incubation with EGF is a Ca(2+)-mediated process that affects trafficking and surface expression of ENaC channels.

Published 26 April 2005 in Biochem Biophys Res Commun, 331(2): 503-11.
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