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PHOSPHOINOSITIDE CYCLE IN DIFFERENTIATION OF TYPE II ALVEOLAR CELLS

In the present study we have evaluated the role of phospholnositide cycle and protein kinase C in signal transmission because INO accelerates maturation of the surfactant system CPed Res 20:1228, 1986). Rabbit lung explants were grown in serum-free medium, and lung epithelial cells (80% of type II cells) cultured in the presence of serum from adult rabbit. - Lung explants from 22-day-old fetuses did not demonstrate surfactant synthesis in the presence of dexamethasone (1 uM) and thyroxlne (1 uM). Phorbol ester or dioctylglycerol increased the synthesis of surfactant ohosphatidylcholine (PC) by 470%, and increased secretion of PC from type II cells by 57%. In the presence of 1.5 mM INO, the hormones alone increased surfactant synthesis & secretion, whereas the activators of protein kinase C did not have a further effect. Addition of fibroblast-pneumonocyte factor into explants labeled with 1.5 mM 3H-INO, transiently decreased dl- and triphosphoinositide labeling. This was evident only when the medium contained high INO C1.5mM). - We propose that protein kinase C transmits signals into very immature alveolar cells and that high extracellular inositol is required for activation of the phosphoinositide cycle, and of protein kinase C.