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Department of Anatomy and Cell Biology, University of Iowa College of Medicine, Iowa City, Iowa 52242
In the human fetal lung, surfactant protein A
(SP-A) is encoded by two highly similar genes, SP-A1 and SP-A2, which
are developmentally and hormonally regulated. Using primer extension
analysis, we evaluated the levels of SP-A1 and SP-A2 mRNA transcripts
in human fetal lung explants and in a human adult lung adenocarcinoma
cell line (H441 cells) cultured in the absence or presence of either dibutyryladenosine 3',5'-cyclic monophosphate (DBcAMP, 1 mM), dexamethasone (10
7 M),
or insulin (2.5 µg/ml). In the human fetal lung explants, the content
of SP-A1 mRNA was approximately four times that of SP-A2 mRNA. DBcAMP
increased SP-A1 mRNA levels by 100% and SP-A2 mRNA levels by 500%,
thus reducing the ratio of SP-A1 mRNA to SP-A2 mRNA to ~1:1.
Dexamethasone inhibited all of the SP-A1 and SP-A2 mRNA transcripts to
the same extent, by ~70%, whereas insulin inhibited all SP-A mRNA
transcripts by ~60%. The ratio of SP-A1 to SP-A2 mRNA in
dexamethasone- or insulin-treated explants was the same as the ratio
observed in controls. In the H441 cells, SP-A1 mRNA levels were ~1.5
times that of SP-A2 mRNA levels. DBcAMP increased both SP-A1 and SP-A2
mRNA levels by 100%. Dexamethasone inhibited SP-A1 mRNA levels in the
cell line by 60%, whereas SP-A2 mRNA levels were not significantly
affected. Insulin inhibited SP-A1 mRNA levels in the cell line by 40%
without affecting SP-A2 mRNA levels. These findings suggest that the
two human SP-A genes are regulated differently in the two model
systems.
lung; surfactant protein A; hormones; gene regulation; adenosine 3',5'-cyclic monophosphate
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