Relative expression of the human epithelial na+ channel (enac) sub
-units in normal and cystic fibrosis airways.
Burch, L. H., C. Talbot, M. R. Knowles, C. Canessa, B. Rossier, R. C.
Boucher.
The University of North Carolina at Chapel Hill, Department of
Medicine, Division of Pulmonary Diseases, and *Universite de
Lausanne, Institut de Pharmacologie et de Toxicologie
APStracts 2:0223C, 1995.
The availability of the newly cloned subunits (,, ) of the epithelial
Na+ channel (ENaC) permits molecular studies of the pathogenesis of
the abnormal Na+ transport rates of CF airway epithelia. Northern
analyses of airway epithelia showed that both normal and CF airway
epithelia express ENaC sub-unit mRNAs in a ratio of >>. In
situ hybridization studies revealed expression of all three ENaC sub
-units in the superficial epithelium, and the and sub-units in the
gland ductular and acinar epithelium of both normal and CF airways.
Ribonuclease protection assays revealed that the steady-state levels
of,, and ENaC mRNAs were similar in CF and normal airway superficial
epithelia. These findings indicate that 1) Na+ transport defects in
CF airways disease may be expressed in glandular acinar and ductal
epithelium as well as superficial epithelium, and 2) the molecular
pathogenesis of Na+ hyperabsorption in CF airways does not reflect
increased levels of Na+ channel mRNAs and probably number, but likely
an absence of the normal inhibitory regulation of Na+ channels by
CFTR proteins.
Received 23 February 1995; accepted in final form 26 May 1995.
APS Manuscript Number C100-5.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 8 June 1995.