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Divisions of 1 Pulmonary Medicine and 2 Pulmonary Biology, Children's Hospital Medical Center, Cincinnati, Ohio 45229-3039
Transgenic mice overexpressing
human transforming growth factor-
(TGF-) develop emphysema and
fibrosis during postnatal alveologenesis. To assess dose-related
pulmonary alterations, four distinct transgenic lines expressing
different amounts of TGF- in the distal lung under control of the
surfactant protein C (SP-C) promoter were characterized. Mean lung
homogenate TGF- levels ranged from 388 ± 40 pg/ml in the
lowest expressing line to 1,247 ± 33 pg/ml in the highest
expressing line. Histological assessment demonstrated progressive
alveolar airspace size changes that were more severe in the higher
expressing TGF- lines. Pleural and parenchymal fibrosis were only
detected in the highest expressing line (line 28), and
increasing terminal airspace area was associated with increasing
TGF- expression. Hysteresis on pressure-volume curves was
significantly reduced in line 28 mice compared with other
lines of mice. There were no differences in bronchoalveolar lavage
fluid cell count or differential that would indicate any evidence of
lung inflammation among all transgenic lines. Proliferating cells were
increased in line 28 without alterations of numbers of type
II cells. We conclude that TGF- lung remodeling in transgenic mice
is dose dependent and is independent of pulmonary inflammation.
pulmonary fibrosis; emphysema; epidermal growth factor receptor
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