Abstract
Addition of PGE 2, but not PGF 2α, to fetal lung organ cultures accelerates the process of self-differentiation with increased dilatation of terminal airsacs and differentiation of the epithelial lining. Indomethacin reduces the endogenous production by organ cultures of PGE 2, PGF 2α, 13,14-dihydro-15-keto-PGE 2, and 13,14-dihydro-15-keto-PGF 2α and retards the process of self-differentiation. Prolonged exposure of cultures to indomethacin results in cell necrosis. Indomethacin inhibition of self-differentiation can be reversed and accelerated by the addition of PGE 2. Addition of PGF 2α in the presence of indomethacin prevents indomethacin-associated cell necrosis but does not accelerate dilatation or differentiation beyond that of cultures in serafree media without additions. We propose that the endogenous production of PGE 2 is a key process in the mechanism of self-differentiation of human fetal lung in organ culture.
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