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Effects of EGF on alveolar epithelial junctional permeability and active sodium transport
Ist Teil von
American journal of physiology. Lung cellular and molecular physiology, 1996-04, Vol.270 (4), p.559-L565
Ort / Verlag
United States
Erscheinungsjahr
1996
Quelle
MEDLINE
Beschreibungen/Notizen
Z. Borok, A. Hami, S. I. Danto, R. L. Lubman, K. J. Kim and E. D. Crandall
Will Rogers Institute of Pulmonary Research Center, University of Southern California, Los Angeles 90033, USA.
We evaluated the effects of epidermal growth factor (EGF) on
transepithelial resistance (Rt) and active ion transport by alveolar
epithelial cell (AEC) monolayers on tissue culture-treated polycarbonate
filters. Rat type II cells were cultured in completely defined serum-free
medium (MDSF) or MDSF supplemented with EGF. The addition of EGF from
either day 0 (chronic) or day 4 (subacute) resulted in significant
increases in Rt and short-circuit current (ISC) on day 5. After subacute
exposure, these effects were delayed in onset by 6-12 h and sustained for
> 24 h. Basolateral (but not apical) EGF was responsible for these
effects, which were prevented by preincubation with tyrphostin RG-50864, a
reversible specific inhibitor of the EGF receptor tyrosine kinase. ISC
decreased, with a sensitivity to apical inhibitors of sodium transport in
the order benzamil > amiloride > 5-(N-ethyl-N-isopropyl) amiloride in
MDSF +/- EGF, and was completely inhibited by the addition of basolateral
ouabain. Net sodium flux and Na+, K+ -ATPase activity both increased
approximately 50% in the presence of EGF. These results indicate that 1)
EGF decreases tight junctional permeability and increases active sodium
transport by AEC monolayers via basolaterally located EGF receptors, and 2)
the pathways for AEC sodium entry and exit (+/- EGF) are apical high
amiloride affinity sodium channels and basolateral sodium pumps.