Differential Influence of Dexamethasone on the Activity and Synthesis of β-Galactoside Specific Lectin (Galaptin) During Postnatal Lung Development

Abstract

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.

Galectin-1 Is Overexpressed in Nasal Polyps under Budesonide and Inhibits Eosinophil Migration

“…Ten-fold overexpression of this gene concurrent with onset of glucocorticoid-induced apoptosis in the susceptible human T cell leukemia line CEM C7 implicates this lectin in glucocorticoid-mediated lymphocytolysis (Goldstone and Lavin, 1991). Regulation of galectin-1 by mechanisms at the level of transcription, translation, or degradation has also been noted during postnatal rat lung development, in which stage and duration of treatment with dexamethasone were found to be critical (Clerch et al, 1987;Sandford et al, 1993). Transcriptional regulation can be attributed to the presence of a putative steroid-binding site located at Ϫ210 in the galectin-1 gene (Gitt and Barondes, 1991).…”

Towards functional glycomics by localization of binding sites for tissue lectins: lectin histochemical reactivity for galectins during diethylstilbestrol-induced kidney tumorigenesis in male Syrian hamster

“…Steroid responsiveness is also seen for glucocorticoids in the human T cell leukemia line CEM C7 and clinical material of nasal polyps (Goldstone and Lavin 1991;Delbrouck et al 2002). Studies on galectin-1 expression in postnatal development of rat lung have indicated that translation and degradation are further levels of regulation by dexamethasone (Clerch et al 1987;Sanford et al 1993). Thus, galectin-1 expression observed in the preneoplastic clusters might be attributed to DES exposure.…”

Heterologous expression of newly identified galectin-8 from sea urchin embryos produces recombinant protein with lactose binding specificity and anti-adhesive activity

“…Thus, multiple signalling pathways and enzymatic cascades are influenced by lectins. Therefore, it is not surprising that certain lectins are expressed in a developmentally regulated fashion, both during early embryonic 3 and postnatal development 4 . A subgroup of lectins is represented by the galectins [previously referred to as ‘S-type lectins’, emphasizing the activity dependence of some of them on thiols (reducing conditions)] 5 .…”