作者: Martin Post , Joanna Floros , Barry T. Smith
DOI: 10.1038/308284A0
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摘要: Fetal lung maturation, especially the onset of surfactant formation by alveolar type II cells, seems to be regulated endogenous fetal glucocorticoids1–3. Recent studies4,5 suggest that glucocorticoids do not act directly on cell but rather mesenchyme. In response glucocorticoids, mesenchyme produces and secretes a polypeptide, fibroblast–pneumonocyte factor, which in turn stimulates synthesis cell6. We report here generation hybridomas secreting monoclonal antibodies rat factor. Two studied detail reduced cortisol-stimulated saturated phosphatidylcholine organotypic cultures cells blocked stimulatory effect fibroblast-pneumonocyte factor from these cultures. When embryonic chicks were injected day 15 incubation with either antibody, they showed days 20 21 biochemical evidence delayed maturation as compared controls. These effects organospecific. Our observations support physiological role for prenatal maturation.