TYPE II PNEUMOCYTE MEMBRANE PHOSPHOLIPID METHYLATION IS NECESSARY FOR SURFACTANT SECRETION

Abstract

Membrane phospholipid methylation has been implicated in membrane receptor signal transmission and cell secretion. In the type II pneumocyte, beta-adrenergic cell membrane receptors are important in initiating secretion of pulmonary surfactant. We studied membrane methyltransferase activity in type II pneumocytes. Type II pneumocytes were purified to near homogeneity from adult rabbit lung and cultured at a density of 3 × 10⁶ cells per culture well. Cells were grown in Eagle MEM with 10% FCS. ³H-1-methionine was utilized as the methyl donor. Phospholipid methylation was stimulated by terbutaline and isuprel, both potent beta-adrenergic agonists, and inhibited by the beta-adrenergic agent propanolol. Methylation was also inhibited by 3-deazoadenosine, a potent methyltransferase inhibitor. For evaluation of surfactant secretion, ³H-choline C1 was added to cultures. Surfactant secretion was stimulated by terbutaline. 3-deazoadenosine inhibited surfactant secretion in response to a beta-adrenergic stimulus. Thus, membrane phospholipid methylation plays a necessary role in surfactant secretion in the type II pneumocyte.

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