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1 Department of Physiology, Monash University, Clayton, Victoria 3168, Australia; and 2 Department of Obstetrics and Gynaecology, University of Western Ontario, London, Ontario, Canada N6A 5A5
Obstruction of the fetal trachea is a potent
stimulus for fetal lung growth, and it has been suggested that this
procedure may be used therapeutically to reverse lung growth deficits
in human fetuses with lung hypoplasia. However, little is known about the effects of increased lung expansion on other aspects of lung development. Our aim was to determine the effect of increased and
decreased lung expansion on the mRNA levels encoding surfactant protein
(SP) A, SP-B, and SP-C in ovine fetal lungs. Lung tissue samples were
collected from fetuses exposed to 2, 4, or 10 days of increased lung
expansion caused by tracheal obstruction. The mRNA levels for SP-A,
SP-B, and SP-C were determined by Northern blot analysis with specific
ovine cDNA probes; SP-A protein levels were determined by Western blot
analysis. Compared with age-matched (128-day gestational age) control
fetuses, SP-A, SP-B, and SP-C mRNA levels in fetal lung tissue were
significantly reduced at 2 days of tracheal obstruction and remained
reduced at 4 and 10 days. However, SP-A protein levels were not reduced
at 2 days of tracheal obstruction, tended to be reduced at 4 days, and
were almost undetectable at 10 days. In contrast to tracheal
obstruction, 7 days of lung liquid drainage significantly increased
SP-C, but not SP-A, mRNA levels in fetal lung tissue compared with
age-matched control fetuses. Our results demonstrate that increases in
fetal lung expansion, induced by obstruction of the fetal trachea,
cause large simultaneous reductions in SP-A, SP-B, and SP-C mRNA levels in the fetal lung as well as a decrease in SP-A protein levels. These
data suggest that expression of the genes encoding SPs in the fetal
lung are specifically responsive to the degree of lung expansion.
messenger ribonucleic acid; fetus; fetal lung liquid; fetal lung liquid volume
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