The epidermal growth factor (EGF) factor family, which includes transforming growth factor α (TGFα), is believed to have a major role in morphogenesis of the fetal lung. We have previously shown that EGF mRNA is significantly decreased in pulmonary hypoplasia due to oligohydramnios(O). We investigated whether the mRNA for TGFα, felt to be a fetal form of EGF, also is significantly decreased in this rat model of fetal lung hypoplasia. We induced O on day 16 in 8 pregnant rat mothers. For half of the fetuses in each litter, the amniotic sacs were punctured and allowed to drain for the remainder of the pregnancy. We harvested the lungs on d 21 and performed RTPCR on TGFα mRNA from the hypoplastic and control lungs. The PCR bands were normalized to β actin PCR bands and converted to densitometric units. The data are mean ± s.e.m.Table

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We conclude that although the lungs are significantly smaller in response to O, TGFα mRNA is significantly and unexpectedly increased in O. This supports our previous findings of increased TGFα protein in hypoplastic lungs, which is in contrast to the decrease in EGF (mRNA and protein) seen subsequent to O. These data would suggest that TGFα and EGF, although closely related, have very different responses to O and may have a different mechanism of action during morphogenesis. We speculate that at this stage of lung development in this model, TGFα may increase in an attempt to stimulate growth, but is unlikely to be the primary stimulus for fetal lung growth.