Endocrinology of the Lung: Development and Surfactant by Carole R. Mendelson

By Carole R. Mendelson

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Boggaram V, Margana RK. Developmental and hormonal regulation of surfactant protein C (SP-C) gene expression in fetal lung: role of transcription and mRNA stability. J Biol Chem 1994;269:27,767–27,772. 62. Veletza SV, Nichols KV, Gross I, Lu H, Dynia DW, Floros J. Surfactant protein C: hormonal control of SP-C mRNA levels in vitro. Am J Physiol 1992;262:L684–L687. 63. Mariencheck W, Crouch E. Modulation of surfactant protein D expression by glucocorticoids in fetal rat lung. Am J Respir Cell Mol Biol 1994;10:419–429.

At 24 wk gestation, when human fetal lung contains appreciable amounts of both SP-B and SP-C mRNAs, little mature SP-B or SP-C protein is detected. Thus, it is likely that expression of specific endoproteases for processing of pro-SP-B and pro-SP-C is a key event in the ontogeny of these proteins. Inherited deficiency of SP-B, which blocks formation of mature SP-C, results in fatal respiratory disease in term infants (158,168). Similarly, monoclonal antibodies to SP-B produce respiratory distress when administered to animals and also inactivate preparations of surfactant that contain SP-B (169,170).

At least 23 different proteins of postnatal lung cells are regulated by glucocorticoids. Recent evidence suggests that many of these antiinflammatory effects of glucocorticoids derive from a direct inhibitory effect of activated GR on the transactivation activity of NFgB, which is a key mediator of inflammatory signals in responsive genes. The surfactant-associated proteins, in particular SP-B and SP-C are essential for normal function of surfactant and consequently normal respiration. All of the surfactant proteins are regulated by glucocorticoids in developing lung and the properties of induction/ repression have been extensively investigated.

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