Differential influence of dexamethasone on the activity and synthesis of beta-galactoside specific lectin (galaptin) during postnatal lung development.

This study examined the regulation of the activity and synthesis of lung beta-galactoside specific lectin (galaptin) by dexamethasone (Dex). The effect of Dex was different depending on the postnatal period administered. Dex decreased galaptin activity and synthesis when administered daily during the "critical period" of alveolarization (postnatal days 3-13) described by Massaro and coworkers (J Clin Invest 76:1297-1305, 1985). The normal rise in galaptin activity (both soluble and membrane- or particulate-bound) observed for untreated controls was prevented by Dex (0.22 mg/pup day-1) treatment. Short-term (2 days) administration on days 4 and 5 had little effect. However, short-term administration of Dex at a later time (days 10-11) increased galaptin activity and synthesis. Both soluble and particulate-bound galaptin were similarly increased by Dex. These studies indicate that both pools of galaptin may be synthesized and activated by a similar mechanism. The effects of Dex on galaptin expression by the postnatal rat lung suggests that endogenous glucocorticoids play a role in the regulation of galaptin activity. The findings for rats given this level of Dex suggest that the period in which exogenous glucocorticoids are administered initially, either as short-term or chronic treatments, is important for the direction of their effect on galaptin expression.